Star epithelocytes - The most numerous cells of intestinal epithelium performing the main absorption intestinal function. These cells make up about 90% of the total number of cell epithelium cells. A characteristic feature of their differentiation is the formation of a brush cut from densely located microvones on the apical surface of the cells. The length of the microwave is about 1 μm, diameter, approximately 0.1 μm.

The total number of microvones on surface One cell ranges over wide range - from 500 to 3000. Microhoversinki are covered with a glycocalix that adsorbs enzymes involved in the interface (contact) digestion. Due to the microvascular, the active surface of the absorption of the intestine increases 30-40 times.

Between epitheliocytes In their apical part, contacts of the type of adhesive belts and dense contacts are well developed. The basal parts of the cells are in contact with the side surfaces of neighboring cells by means of interdagitations and despair, and the base of the cells is attached to the basal membrane of semi-mosmos. Due to this system of intercellular contacts, intestinal epithelium performs an important barrier function, preventing the organism from penetration of microbes and alien substances.

Box-shaped exocrinocytes - This is essentially unicellular mucous glands, located among the columnar epitheliocytes. They produce carbohydrate-protein complexes - mucins that perform a protective function and promoting food in the intestine. The number of cells increases towards the distal intestinal department. The shape of the cells changes to various phases of the secretory cycle from the prismatic to the glass-shaped. In the cytoplasm of cells, the Golgi complex and the granular endoplasmic network are developed - the centers of the synthesis of glycosaminoglycans and proteins.

Patenet cells, or exocrinocytes with acididophilic granules, are constantly in crypta (6-8 cells) of the skinny and iliac intestine. The total number of their approximately 200 million in the apical part of these cells is determined by acidophilic secretory granules. A zinc is also detected in the cytoplasm, a well-developed granular endoplasmic network. Cells allocate the secret rich in the enzyme peptidase, lysozyme, etc. It is believed that the secret of cells neutralizes the salt acid of the intestinal content, participates in the splitting of dipeptides to amino acids, has antibacterial properties.

Endocrinocytes (Enterochromafinocytes, argenufacthythphine cells, Cells of Kulchitsky) - basalneous cells located at the bottom of Krypt. They are well impregnated with silver salts, have affinity for chromium salts. Among endocrine cells there are several species secreting various hormones: EU cells produce melatonin, serotonin and substance P; S-cells - secretine; ECL cells - enteroglukgon; I-cells - cholecystokinin; D-cells - produce somatostatin, VIP - vasoactive intestinal peptides. Endocrinocytes are about 0.5% of the total number of cells of the intestinal epithelium.

Updated these cells are much slower than epithelocytes. The methods of histoadioavatography have been established a very rapid update of the cell composition of the intestinal epithelium. It happens for 4-5 days in the duodenum and a little slower (for 5-6 days) in the ileum.

Owl plate mucous membrane The small intestine consists of loose fibrous connective tissue, in which macrophages, plasma cells and lymphocytes are determined. There are also similar (solitary) lymphatic nodules and larger clusters of lymphoid tissue - aggregates, or group lymph nodes (plaque peaers). The epithelium covering the latter has a number of features of the structure. Its composition contains epithelocytes with microslides on the apical surface (M cells). They form endocytomic vesicles with an antigen and exocytosis translate it into the intercellular space where lymphocytes are located.

Subsequent development I. the formation of plasma cellsThe development of them Immunoglobulins neutralizes antigens and intestinal content microorganisms. Muscular mucosa plate is represented by a smooth muscular cloth.

In submucosal based duodenal gut There are duodenal (brunner) gland. These are complex branched tubular mucous glands. The main type of cells in the epithelium of these glands - mucous glandulocytes. The output ducts of these glands are laid out by the cacular cells. In addition, in the epithelium of the duodenal glands there are cells of the PAnet, glass-shaped exocrinocytes and endocrinocytes. The secret of these glands is involved in the splitting of carbohydrates and neutralization of hydrochloric acid coming from the stomach, mechanical protection of the epithelium.

Muscle sheath of the small intestine It consists of internal (circular) and outdoor (longitudinal) layers of smooth muscle tissue. In the twelfth gum, the muscle cake is subtle and due to the vertical location of the intestine practically does not participate in the peristalsis and promotion of Himus. Outside, the small intestine is covered with a serous shell.

In the small intestine, duodenum, skinny and iliac intestine are distinguished. The duodenum not only participates in the secretion of intestinal juice with a high content of hydrocarbonate ions, but also is the dominant zone of regulating the digestion. It is the duodenum that defines a certain rhythm distal departments digestive tract Through the nervous, humoral and intra-palm mechanisms.

Together with the anthral stomach department, the duodenal, skinny and iliac guts make an important single endocrine organ. The duodenum is part of a contractile (motor) complex, as a whole, consisting of an anthral ventricular, a pylorical canal, duodenum and a sphincter Oddi. It takes the acidic contents of the stomach, highlights its secrets, changes the pH of the Hamus in the alkaline side. The contents of the stomach acts on endocrine cells and nerve endings of the duodenum mucosa, which provides the coordinating role of the anthral stomach and duodenal sector, as well as the relationship between the stomach, pancreas, liver, the small intestine.

Outside digestion, an empty stomach, the contents of the duodenum has a weakly alkaline reaction (pH 7.2-8.0). When moving into its portions of acidic content from the stomach, the reaction of duodenal content also becomes acidic, but then it quickly changes its change, since the hydrochloric acid of the gastric juice is neutralized here with bile, pancreatic juice, as well as duodenal (brunner) glands and intestinal crypt (Librics ). In this case, the effect of gastric pepsin stops. The higher the acidity of the duodenal content, the greater the pancreatic and bile juice and the greater the evacuation of the contents of the stomach in the duodenum slows down. In the hydrolysis of nutrients in the duodenum, the role of the enzymes of the pancreas juice, bile, is especially great.

The digestion in the small intestine is the most important stage of the digestive process as a whole. It provides the depolymerization of nutrients to the stage of monomers, which are absorbed from the intestine to blood and lymph. The digestion in the small intestine occurs first in its cavity (strip digestion), and then in the zone of the brush border of the intestinal epithelium with the help of enzymes embedded in the microwave microwave membrane, as well as fixed in glycicalce (membrane digestion). Hanging and membrane digestion is carried out by enzymes coming with pancreatic juice, as well as actually intestinal enzymes (membrane, or transmembrane) (see Table 2.1). An important role in splitting lipids is playing bile.

For a person, a combination of a curb and membrane digestion is most characteristic. The initial stages of hydrolysis are carried out due to extension digestion. Most of the supramolecular complexes and large molecules (proteins and products of their incomplete hydrolysis, carbohydrates, fats) are split into the cavity of the small intestine in neutral and weakly alkaline media, mainly under the action of endohydrolases secreted by the pancreas cells. Some of these enzymes can be adsorbed on mucus structures or mucous overlauses. The peptides formed in the proximal intestine and consisting of 2-6 amino acid residues are given 60-70% -amicoism, and in the distal part of the intestine - up to 50%.

Carbohydrates (polysaccharides, starch, glycogen) are cleaved by -amilate pancreatic juice to dextrins, three and disaccharides without significant glucose accumulation. Fats are subjected to hydrolysis in cavity with pancreatic lipase, which gradually clears fatty acids, which leads to the formation of di- and monoglycerides, free fatty acids and glycerol. In the hydrolysis of fats, bile plays a significant role.

The products of partial hydrolysis produced in the cavity of the small intestine, thanks to the intestinal motility, comes from the cavity of the small intestine to the brush border zone, which contributes to their transfer in the streams of the solvent (water) arising due to the suction of sodium and water ions. It is on the structures of a brush kayma and a membrane digestion occurs. In this case, the intermediate stages of hydrolysis of biopolymers are implemented by pancreatic enzymes adsorbed on the structures of the apical surface of enterocytes (glycocalcalis), and the final - actually intestinal membrane enzymes (Maltazua, Sakharase, isomaltase, carriage, aminoptidase, tri- and dipeptidases, alkaline phosphatase, monoglyceridalipase et al.)\u003e Enterocytes built into the membrane, covering the microwave brush kayma. Some enzymes (-amilases and aminopeptidase) hydrolyzed and highly polware products.

The peptides entering the brush border of intestinal cells are cleaved to oligopeptides, dipeptides and amino acids capable of suction. Peptides consisting of more than three amino acid residues are hydrolyzed predominantly enzymes of brush border, and three and dipeptides are both brush border enzymes and intracellularly enzymes of the cytoplasm. Glycylglicin and some dipeptides containing the remains of proline and oxyproline and have no significant nutritional values, are separated partially or completely in an unrehacled form. Disaccharides coming with food (for example, sucrose), as well as the starch and glycogen formed during the splitting of starch and glycogen, are hydrolyzed by intestinal glycosidases to monosaccharides, which are transported through the intestinal barrier to the inner medium. Triglycerides are split not only under the action of pancreatic lipase, but also under the influence of intestinal monoglyceridlipase.

Secretion

In the mucous membrane of the small intestine there are ferrous cells located on vile, which produce digestive secrets that are distinguished by the intestine. This is the Brunner of the Blue of the duodenum, Liborkyunov Crypts of the Torky, Wildlife Cells. Endocrine cells produced hormones that enter the intercellular space, and where they are transported in lymph and blood. Here the cellular cells with acidophilic granules in the cytoplasm (PAnet cells) are localized here. The volume of intestinal juice (normally up to 2.5 liters) may increase with the local exposure of some food or toxic substances on the intestinal mucosa. The progressive dystrophy and atrophy of the mucous membrane of the small intestine is accompanied by a decrease in the secretion of intestinal juice.

The glandular cells form and accumulate the secret and at a certain stage of their activities are rejected into the intestinal lumen, where, decaying, give this secret into the surrounding fluid. Juice can be divided into liquid and dense parts, the ratio between which changes depending on the strength and nature of the irritation of intestinal cells. The liquid part of the juice contains about 20 g / l of dry matter, consisting partially from the contents of deskvamated cells coming from the blood of organic (mucus, proteins, urea, etc.) and inorganic substances - approximately 10 g / l (such as bicarbonates, chlorides, phosphates). The dense part of the intestinal juice has the form of mucous lumps and consists of non-destructive deskvamated epithelial cells, fragments and mucus (secrets of glassoid cells).

In healthy people, periodic secretion is characterized by relative qualitative and quantitative stability, which contributes to maintaining the homeostasis of the enteral medium, which is primarily a chimus.

According to some calculations, an adult with digestive juices enters up to 140 g of protein per day, another 25 g of protein substrates is formed as a result of the desquamation of intestinal epithelium. It is not difficult to present the significance of protein losses that can occur with a long and heavy diarrhea, with any forms of digestive disorders, pathological conditions associated with enteral insufficiency - enhanced sublock secretion and impaired reverse absorption (reabsorption).

The mucus synthesized by glass-shaped cells of the small intestine is an important component of secretory activity. The number of glazing cells in the composition of the villi is greater than in the crypta (approximately 70%), and increases in the distal sections of the small intestine. Apparently, this reflects the importance of non-oxide mucus functions. It has been established that the cellular epithelium of the small intestine is coated with a solid heterogeneous layer with a thickness of up to 50-fold height of enterocyte. In this overpithelial layer of mucous overlays, there is a significant amount of adsorbed pancreatic and minor number of intestinal enzymes that implement the digestive function of the mucus. The mucous secret is rich in acidic and neutral mucopolysaccharides, but poor proteins. This provides the cytoprotective consistency of the mucous gel, mechanical, chemical protection of the mucous membrane, preventing the penetration into the deep structure of the tissue of large-molecular compounds and antigenic aggressors.

Suction

Under the absorption, the combination of processes is understood, as a result of which the components of food contained in the digestive cavities are transferred through the cellular layers and the intercellular paths into the internal circulatory mediums of the body - blood and lymph. The main gut is the main gut, although some nutritional components can be absorbed in the colon, stomach and even the oral cavity. Foods coming from the small intestine, with a blood current and lymphs are distributed throughout the body and then participate in intermediate (intermediate) exchange. A day in the gastrointestinal tract is absorbed to 8-9 liters of liquid. Of these, approximately 2.5 liters come with food and drink, the rest is the liquid of the secrets of the digestive apparatus.

The absorption of most food substances occurs after their enzymatic treatment and depolymerization, which occur both in the cavity of the small intestine and on its surface due to membrane digestion. Already after 3-7 hours after meals, all its main components disappear from the cavity of the small intestine. The intensity of the absorption of foodstuffs in various parts of the small intestine is noonail and depends on the topography of the corresponding enzymatic and transport activity along the intestinal tube (Fig. 2.4).

There are two types of transport through the intestinal barrier into the inner medium of the body. This is a transmembrane (transcellular, through a cell) and paracellular (shunting, going through intercellular spaces).

The main type of transport is transmembrane. It is possible to distinguish two types of transmembrane transfer of substances through biological membranes - it is macromolecular and micromolecular. Under macromolecular transportit is understood by the transfer of large molecules and molecular aggregates through cell layers. This transport is intermittent and is implemented mainly by pin and phagocytosis, united by the name "endocytosis". Due to this mechanism, proteins can flow, including antibodies, allergens and some other compounds, meaningful to the body.

Micromolecular transportserves as the main type, as a result of which foodstuff hydrolysis products are transferred from the intestinal environment in the inner medium of the body, mainly monomers, various ions, medications and other compounds with a small molecular weight. The transport of carbohydrates through the plasma membrane of intestinal cells occurs in the form of monosaccharides (glucose, galactose, fructose, etc.), proteins are predominantly in the form of amino acids, fats - in the form of glycerol and fatty acids.

During the transmembrane movement, the substance crosses the membrane microwaves of the brush border of intestinal cells, enters the cytoplasm, then through the basolateral membrane to the lymphatic and blood vessels of intestinal veins and further into the general circulation system. The cytoplasma of intestinal cells serves as a compartment forming the gradient between the brush border and the basolateral membrane.

Fig. 2.4. The distribution of resorbative functions along the small intestine (by: S. D. Booth, 1967, as amended).

In micromolecular transport, in turn, it is customary to allocate passive and active transport. Passive transport can occur due to diffusion of substances through a membrane or aqueous pores along a concentration gradient, osmotic or hydrostatic pressure. It accelerates thanks to moving through the pores of water flows, changes in the pH gradient, as well as conveyors in the membrane (in case of lightweight diffusion, their work is carried out without energy costs). Exchange diffusion provides microcirculation of ions between the periphery of the cell and the surrounding microne. Light diffusion is implemented with the help of special conveyors - special protein molecules (specific transport proteins) that contribute to the penetration of substances through the cell membrane at the expense of the concentration gradient.

Actively transported substancemoves through the apical membrane of the intestinal cell against its electromechanical gradient with the participation of special transport systems operating by type of mobile or conformational conveyors (carriers) with considerable energy. This active transport is sharply different from lightweight diffusion.

Vehicles of most organic monomers through the membrane of the brush border of intestinal cells depends on sodium ions. This is true for glucose, galactose, lactate, most amino acids, some conjugated bile acids, as well as for a number of other connections. The driving force of such transport is the Gradient of the concentration of Na +. However, in the cells of the small intestine, there is not only Ma + dependent transport system, but also ma +--independent, which is characteristic of some amino acids.

Waterit is absorbed from the intestine to the blood and comes back according to the laws of osmosis, but most of the isotonic solutions of the intestinal chimus, since in the intestine hyper and hypotonic solutions are quickly bred or concentrated.

Suction sodium ionsin the intestines occurs both through the basolateral membrane into the intercellular space and further into the blood and the transcellular means. During the day, the person's digestive tract comes with food 5-8 g sodium, 20-30 g of this ion is secreted with digestive juices (i.e., only 25-35 g). Sodium ions are absorbed together with chlorine ions, as well as during the opposite directional transport of potassium ions due to Na +, K + -atphase.

Suction of bivalent ions(Ca2 +, Mg2 +, Zn2 +, Fe2 +) occurs along the entire length of the gastrointestinal tract, and S2 + is mainly in the stomach. Bivalent ions are absorbed very slowly. The absorption of CA2 + is most actively occurring in duodenum and skinny intestines with the participation of simple and light diffusion mechanisms, activated by vitamin D, pancreatic juice, bile and a number of other connections.

Carbohydratesabsorbed in a small intestine in the form of monosaccharides (glucose, fructose, galactose). The absorption of glucose occurs actively with the cost of energy. Currently, a molecular structure No. +-dependent glucose conveyor is already known. This is a protein oligomer with high molecular weight and extracellular loop, which has glucose and sodium binding centers.

Proteinsthey are absorbed through the apical membrane of intestinal cells preferably in the form of amino acids and to a much lesser extent in the form of dipeptides and tripipeptides. As in the case of monosaccharides, the energy for transport of amino acids is provided by a sodium kitransporter.

In the brush border of enterocytes, there are at least six Na +-dependent transport systems for various amino acids and three-independent sodium. Peptide (or amino acid) conveyor, as well as glucose conveyor, is an oligomeric glycosylated protein with an extracellular loop.

As for the suction of peptides, or the so-called peptide transport, then in the early periods of postnatal development in the small intestine there is absorption of intact proteins. Currently, it is accepted that in general the absorption of intact proteins is the process of physiological, necessary for the selection of antigens by subepithelial structures. However, against the background of the overall admission of food proteins, this process is mostly in the form of amino acids has a very small nutritional value. A number of dipeptides can flow into the cytoplasm with transmembrane, as well as some tripipes, and split intracellularly.

Transport Lipidit is carried out differently. Formed in the hydrolysis of fatty foods, long-chain fatty acids and glycerin are practically passively transferred through the apical membrane to enterocyte, where they are reintezed in triglycerides and consist in a lipoprotein shell, the protein component of which is synthesized in enterocyte. Thus, a chilomicron is formed, which is transported to the central lymphatic vessel of intestinal villus and on the system of the breast lymphatic duct then enters the blood. Middle-chain and short-chain fatty acids enter the bloodstream immediately, without resintez triglycerides.

The absorption rate in the small intestine depends on the level of its blood supply (affects the processes of active transport), the level of intracean pressure (affects the filtration processes from the intestinal lumen) and the topography of suction. Information about this topography makes it possible to imagine the features of the absorption deficiency in enteral pathology, during pre-section syndromes and other disorders of the gastrointestinal tract. In fig. 2.5 Presented a scheme for monitoring processes occurring in the gastrointestinal tract.

Fig. 2.5. Factors affecting the secretion and absorption processes in the small intestine (by: R. J. Levin, 1982, as amended).

Motorika

Motor-evacuation activity is essential for digestive processes in the small intestine, which provides mixing of food content with digestive secrets, the promotion of chimus in the intestine, shift the chimus layer on the surface of the mucous membrane, increasing the intranicated pressure, which contributes to the filtering of some chims components from the gut cavity to blood and lymph. Motor activity of the small intestine consists of unsophisticated mixing movements and transmitted peristaltics. It depends on the own activity of smooth muscle cells and from the influence of the vegetative nervous system and numerous hormones, mainly gastrointestinal origin.

So, the reduction in the small intestine occurs as a result of coordinated movements of the longitudinal (outer) and transverse (circulatory) layers of fibers. These reductions may be several types. According to the functional principle, all reductions are divided into two groups:

1) local, which provide mixing and rubbing the contents of the small intestine (impropulusless);

2) aimed at movement of the contents of the intestine (permanent). Several types of abbreviations are distinguished: rhythmic segmentation, pendulum, peristaltic (very slow, slow, fast, rapid), antiperistaltic and tonic.

Rhythmic segmentationprovided mainly to reduce the circulatory layer of muscles. In this case, the contents of the intestine is divided into parts. The next reduction is formed by a new segment of the intestine, the contents of which consists of parts of the former segment. This is achieved by mixing chimus and increase the pressure in each of the forming segments of the intestine. Peal-shaped abbreviationsprovided by reductions of the longitudinal layer of muscles with the participation of circulatory. With these abbreviations, Himus is moving forward-back and a weak progressive movement in the aboral direction. In the proximal divisions of the small intestine, the frequency of rhythmic cuts, or cycles is 9-12, in distal - 6-8 in 1 min.

Peristalsisit is that above Hamus due to a reduction in the circulatory layer of muscles, interception is formed, and below as a result of the reduction of the longitudinal muscles - the expansion of the cavity. This interception and expansion move along the intestine, moving a portion of Himus ahead of the interception. In the length of the intestine, several peristaltic waves are moving at the same time. For antiperistaltic abbreviationsthe wave moves in the opposite (oral) direction. Normally, the small intestine is not reduced by antiperistaltically. Tonic abbreviationsmay have a small speed, and sometimes do not spread at all, significantly narrowing the intestinal lumen at the high distance.

A certain role of motility was revealed in the removal of digestive secrets - the peristalsis of the ducts, the change in their tone, the closure and disclosure of their sphincters, the reduction and relaxation of the gallbladder. To this, changes in the folding of the mucous membrane, micromotoric of intestinal villi and microwaves of the small intestine should be added - very important phenomena that optimize membrane digestion, absorption of nutrients and other substances from the intestine in blood and lymph.

Motoric fine intestine is regulated by nervous and humoral mechanisms. The coordinating influence is intramural (in the intestinal wall) nerve formations, as well as the central nervous system. Intramural neurons provide coordinated intestines. Especially great their role in peristaltic abbreviations. Extrampical, parasympathetic and sympathetic nerve mechanisms, as well as humoral factors, have an influence of intramural mechanisms.

Motor activity of the intestine depends on the physical and chemical properties of the chimus. Increases its activity rude food (black bread, vegetables, coarse fiber products) and fats. With an average movement rate of 1-4 cm / min, food reaches a blind intestine in 2-4 hours. The duration of the displacement of food affects its composition, depending on it the movement speed decreases in a row: carbohydrates, proteins, fats.

Humoral substances change the intestine motorcy, acting directly on muscle fibers and through the receptors on neurons of the intramural nervous system. Strengthening motility of the small intestine Vasopressin, oxytocin, bradykinin, serotonin, histamine, gastin, motilin, cholecystokinin-panopozimine, substance P and a number of other substances (acids, alkalis, salts, food digestive products, especially fats).

Protective systems

Food receipt in the CT should be considered not only as a way of replenishing energy and plastic materials, but also as allergic and toxic aggression. The power is associated with the danger of penetration into the inner medium of various kinds of antigens and toxic substances. Special danger represent alien proteins. Only due to the complex protection system, the negative sides of the power are effectively neutralized. In these processes, a particular intention plays a particularly important role, performing several vital functions - digestive, transport and barrier. It is in a small intestine that is subjected to multi-stage enzymatic processing, which is necessary for subsequent suction and assimilation of the formed hydrolysis products of food substances that have no species specificity. This organism prevents itself to a certain extent from the impact of alien substances.

Barrier or protective, the function of the small intestine depends on its macro and microstructure, an enzyme spectrum, immune properties, mucus, permeability, etc. The mucous membrane of the small intestine is involved in mechanical, or passive, as well as in the active protection of the body from harmful substances. Non-immune and immune mechanisms for the protection of the small intestine protect the inner medium from foreign substances, antigens and toxins. Sour gastric juice, digestive enzymes, including protease of the gastrointestinal tract, a motility of the small intestine, its microflora, mucus, brush border and glycocalix of the apical part of intestinal cells belong to non-specific protective barriers.

Due to the ultrastructure of the surface of the small intestine, that is, the brush border and glycocalcas, as well as the lipoprotein membrane, intestinal cells serve as a mechanical barrier, preventing the admission of antigens, toxic substances and other high molecular compounds from the enteral medium to the internal. The exceptions are molecules subjected to hydrolysis enzymes adsorbed on glycicalis structures. Large molecules and supramolecular complexes can not penetrate the brush border zone, as its pores, or intercraceing spaces, are extremely small. So, the smallest distance between microvils on average is 1-2 microns, and the dimensions of the cells of the glycocalce network are hundreds of times less. Thus, the glycocalix serves as a barrier determining the permeability of food substances, and the apical membrane of intestinal cells due to glycicalis is practically unavailable (or a little accessible) for macromolecules.

To another mechanical, or passive, protection system includes limited permeability of the mucous membrane of the small intestine for water-soluble molecules with a relatively small molecular weight and impermeability for polymers, including proteins, mucopolysaccharides and other substances with antigenic properties. However, for the cells of the digestive apparatus during early postnatal development, endocytosis is characterized, contributing to the intake of macromolecules and alien antigens into the internal environment. Intestinal cells of adult organisms are also capable of absorbing large molecules in certain cases, including non-separable. In addition, during the passage of food through the thin intestine, a significant amount of volatile fatty acids is formed, one of which is caused by toxic effect during suction, while the other is a local irritant effect. As for xenobiotics, their formation and suction in the small intestine varies depending on the composition, properties and contamination of food.

The immunocompetent lymphatic tissue of the small intestine is about 25% of its entire mucous membrane. In anatomical and functional relationship, this tissue of the small intestine is divided into three departments:

1) Peyer plaque - clusters of lymphatic follicles, in which antigens gather and produced by antibodies to them;

2) lymphocytes and plasma cells producing secretory IgA;

3) intraepithelial lymphocytes, mostly T-lymphocytes.

Peyer plaque (about 200-300 in an adult) consist of organized clusters of lymphatic follicles, in which the predecessors of the lymphocyte population are located. These lymphocytes populate other areas of the intestinal mucous membrane and take part in its local immune activities. In this regard, Peyer plaque can be considered as an area initiating the immune activity of the small intestine. Peyer plaque contains in both T-cells, and a small number of M-cells are localized in the epitheliums over plaques, or membrane cells. It is assumed that these cells are involved in the creation of favorable conditions for accessing luminary antigens to subepithelial lymphocytes.

Interpoithelial cells of the small intestine are located between intestinal cells in the basal part of the epithelium, closer to the baseal membrane. Their attitude to other intestinal cells is approximately 1: 6. About 25% of interpoithelial lymphocytes have T-cell markers.

In the mucous membrane of the small intestine of a person there is more than 400 plasma cells per 1 mm2, as well as about 1 million lymphocytes per 1 cm2. Normally, in the current intestine, contains from 6 to 40 lymphocytes per 100 epithelial cells. This means that in the small intestine in addition to the epithelial layer, separating the enteral and inner medium of the body, there is still a powerful leukocytar layer.

As noted above, the intestinal immune system meets a huge number of exogenous food antigens. Cells of fine and large intestines produce a number of immunoglobulins (Ig A, Ig E, Ig G, Ig M), but mainly Ig A (Table 2.2). Immunoglobulins a and e, secreted in the cavity of the intestine, apparently adsorbed on the structures of the intestinal mucous membrane, creating an additional protective layer in the region of glycicalis.

Table 2.2. The number of cells of thin and colon producing immunoglobulins

The functions of a specific protective barrier also performs a mucus that covers most of the epithelial surface of the small intestine. This is a complex mixture of different macromolecules, including glycoproteins, water, electrolytes, microorganisms, descormed intestinal cells, etc. Muzin - a component of the mucus, imparting gelness, contributes to the mechanical protection of the apical surface of intestinal cells.

There is another important barrier warning of the intake of toxic substances and antigens from enteric into the inner medium of the body. This barrier can be called transformationalor enzymatic, as it is due to the enzyme systems of the small intestine, carrying out consistent depolymerization (transformation) of food poly and oligomers to monomers capable of disposal. The enzymatic barrier consists of a number of separate spatially separated barriers, but in general, forms a single interconnected system.

Pathophysiology

In medical practice, disorders of the functions of the small intestine are often found. They are not always accompanied by a distinct clinical symptomatomy and are sometimes masked by extraordinary disorders.

By analogy with the adopted terms ("heart failure", "renal failure", "liver failure", etc.), according to many authors, it is advisable to disrupt the functions of the small intestine, its insufficiency, meaning the term "Enteral insufficiency"(" Fine intestinal failure "). Under enteral insufficiency, it is customary to understand the clinical syndrome due to impaired functions of the small intestine with all their intestinal and extraintestinal manifestations. Enteral failure arises in the pathology of the finest intestine, as well as various diseases other organs and systems. With congenital primary forms of deficiency of the small intestine, the isolated selective digestive or transport defect is most often inherited. With the forms acquired, multiple digestion and suction defects are dominated.

The large portions of gastric content entering the duodenum are worse than soaked with duodenal juice and slowly neutralized. Duodenal digestion suffers and because in the absence of free hydrochloric acid or with its deficiency, the synthesis of secretine and cholecystokinin, regulating the secretory activity of the pancreas, is significantly oppressed. The decrease in the formation of pancreatic juice in turn leads to intestinal digestion disorders. This is the reason that the chimus in the suction form is not prepared for suction enters the underlying ports of the small intestine and irritates the receptors of the intestinal wall. There is a strengthening of the peristaltic and secretion of water into the intestinal tube clearance, diarrhea and enteral failure develops as a manifestation of severe digestive disorders.

In the conditions of hypochlorohydria, and especially Ahilia, the absorption function of the intestine is sharply deteriorated. There are violations of protein exchange, leading to dystrophic processes in many internal organs, especially in heart, kidneys, liver, muscle tissue. Disorders may develop immune system. Gastrogen enteral failure early leads to hypovitaminosis, a deficiency in the organism of mineral salts, disorders of homeostasis and a coagulating blood system.

In the formation of enteric insufficiency, violations of the secretory function of the intestine have a certain value. Mechanical irritation of the mucous membrane of the small intestine sharply increases the release of the liquid part of the juice. Not only water and low molecular weight substances, but also proteins, glycoproteides, lipids are stiguously secreted into the small intestine. The described phenomena, as a rule, are developing with sharply oppressed acid formation in the stomach and defective in connection with this intragastric digestion: the undequired components of the food lumps cause sharp irritation of the receptors of the mucous membrane of the small intestine, initiating secretion enhancing. Similar processes occur in patients who suffered resection of the stomach, including the pyloric sphincter. Loss of the reservoir function of the stomach, inhibition of gastric secretion, some other postoperative disorders contribute to the development of the so-called "discharge" syndrome (dumping syndrome). One of the manifestations of this postoperative disorder is the strengthening of the secretory activity of the small intestine, its hypermotorics, manifestable in a diarrhea of \u200b\u200ba subtlety type. The inhibition of intestinal juice products, developing under a number of pathological conditions (dystrophy, inflammation, atrophy of the mucous membrane of the small intestine, ischemic disease of the digestive organs, protein-energy failure of the body, etc.), the decrease in enzymes is the pathophysiological basis of the intestinal secretory disorders. When decreasing the effectiveness of intestinal digestion, the hydrolysis of fats and proteins in the cavity of the small intestine changes little, since the secretion of lipase and proteases with pancreatic juice compensatory increases.

The greatest importance defects of digestive and transport processes have people with congenital or acquired enzympathydue to the lack of certain enzymes. Thus, as a result of lactase deficiency in the cells of the intestinal mucosa, the membrane membrane hydrolysis and the absorption of milk sugar (dairy intolerance, lactase failure) is disturbed. Insufficient products by cells of the mucous membrane of the small intestine of the sacrament, -amilases, malalhazes and isomaltase leads to the development of the intolerance to patients, respectively, sucrose and starch. In all cases of intestinal enzymatic deficit with incomplete hydrolysis of food substrates, toxic metabolites are formed, provoking the development of severe clinical symptoms, not only characterizing the increase in manifestations of enteric insufficiency, but also extintestinal disorders.

With various diseases of the gastrointestinal tract, there are disorders of a strip and membrane digestion, as well as suction. Disorders may have infectious and noncommunicable etiology, being acquired or hereditary. Defects of membrane digestion and suction occur in violations of the distribution of enzymatic and transport activity along the small intestine after, for example, operational interventions, in particular after resection of the small intestine. The pathology of the membrane digestion may be due to the atrophy of the veins and microvascular, violation of the structure and ultrastructure of intestinal cells, a change in the spectrum of the enzyme layer and the sorption properties of the structures of the intestinal mucous membrane, intestinal motility disorders, in which the transfer of food cavities on its surface is disturbed, with IT dysbiosis . d.

Disorders of membrane digestion are found with a rather wide range of diseases, as well as after intensive therapy with antibiotics, various surgical interventions on the gastrointestinal tract. With many viral diseases (poliomyelitis, pig, adenovirus flu, hepatitis, cortex) There are severe disorders of digestion and suction with diarrhea and steatonea phenomena. With these diseases, severe atrophy of the villi, violation of the ultrastructure of the brush border, the insufficiency of the enzyme layer of the intestinal mucous membrane, leading to disorders of membrane digestion.

Often, the violation of the ultrastructure of the brush kayma is combined with a sharp decrease in enzymatic activity of enterocytes. There are numerous cases in which the ultrastructure of the brush kayma remains almost normal, but nevertheless the insufficiency of one or more digestive intestinal enzymes is found. Many food intolerance are due to these specific disorders of the enzyme layer of intestinal cells. Currently, partial enzyme deficiencies of the small intestine are widely known.

Disaccharidase insufficiency (including saccharase) can be primary, that is, due to the corresponding genetic defects, and secondary, developing against the background of various diseases (SPRU, enteritis, after operational interventions, with infectious diarrhea, etc.). Isolated sacrament failure is rare and in most cases is combined with changes in the activity of other disaccharides, most often isomaltase. The lactase insufficiency is especially widespread, as a result of which milk sugar (lactose) is not absorbed and intershotomy to milk occurs. Lactase insufficiency is determined by genetically recessively. It is assumed that the degree of repression of the lactase gene is associated with the history of this ethnic group.

Enzymatic lack of intestinal mucous membrane can be associated both with a violation of the synthesis of enzymes in intestinal cells, and with impaired embedding them into the apical membrane, where they perform their digestive functions. In addition, they may be caused by the acceleration of the degradation of the respective intestinal enzymes. Thus, for the proper interpretation of a number of diseases, it is necessary to take into account disorders of membrane digestion. Defects of this mechanism lead to changes in the receipt of necessary food substances into the body with far-reaching consequences.

The cause of disorders of protein assimilation may be changes in the gastric phase of their hydrolysis, however, the defects of the intestinal phase due to the failure of pancreatic and intestinal membrane enzymes are more serious. Rare genetic disorders include enteropeptidase and tripsis failure. The decrease in peptidase activity in the small intestine is observed under a number of diseases, for example, the incurable form of celiac disease, Crohn's disease, a duodenal ulcer, for radio and chemotherapy (for example, 5-fluorouracyl), etc., and so on splitting the proline peptides inside intestinal cells.

Many disorders of the intestinal functions at various forms of pathology may depend on the state of glycicalis and the digestive enzymes contained in it. Violations of the adsorption processes of pancreatic enzymes on the structures of the mucous membrane of the small intestine may be the cause of small (power failure), and the atrophy of glycocalca can contribute to the damaging effect of toxic agents on the enterocyte membrane.

Disorders of suction processes are manifested in their slowdown or pathological strengthening. The slowing down of the absorption of the intestinal mucous membrane may be due to the following reasons:

1) the insufficient splitting of the dietary masses in the cavities of the stomach and the small intestine (impaired digestion);

2) disorders of membrane digestion;

3) congestive hyperemia of the intestinal wall (vessels paresis, shock);

4) of the ischemia of the intestinal wall (atherosclerosis of the vessels of the mesentery, the scar postoperative occlusion of the vessels of the wizard of the intestine, etc.);

5) inflammation of the tissue structures of the wall of the small intestine (enteritis);

6) resection most of the small intestine (short-sink syndrome);

7) obstruction in upper departments The intestines when the nutritionals do not come to his distal departments.

Pathological enhancement of suction is associated with an increase in the permeability of the intestinal wall, which can often be observed in patients with a disorder of thermoregulation (thermal lesions of the body), infectious-toxic processes under a number of diseases, food allergies, etc. Under the influence of some factors, the threshold of the permeability of the mucous membrane of the small intestine large-molecular compounds, including products of incomplete splitting of food substances, proteins and peptides, allergens, metabolites. The appearance in the blood, in the inner environment of the body of alien substances contributes to the development of general phenomena of intoxication, sensitizing the body, the occurrence of allergic reactions.

It is impossible not to mention such diseases in which the absorption of neutral amino acids in the small intestine, as well as cystinuria. Cystinuria observes combined disorders of the transport of diaminomocarboxylic acids and cystine in the small intestine. In addition to these diseases, there are such as isolated Methionine Malabsorption, tryptophan and a number of other amino acids.

The development of enteral failure and its chronic flow contributes (due to the violation of the processes of membrane digestion and suction) the emergence of disorders of protein, energy, vitamin, electrolyte and other types of metabolism with appropriate clinical symptoms. The noted mechanisms for the development of digestive failure are ultimately implemented in a polyorgan, multisindrome picture of the disease.

In the formation of pathogenetic mechanisms of enteral pathology, the acceleration of the peristaltics is one of the typical disorders accompanying the majority of organic diseases. Most frequent reasons Acceleration of peristaltics - inflammatory changes in the mucous membrane of the gastrointestinal tract. At the same time, Himus moves the intestine faster and develops diarrhea. Diarrhea also occurs under action on the intestinal wall of unusual stimuli: undigested food (for example, with Ahilia), fermentation products and rotting, toxic substances. The acceleration of the peristaltic is to increase the excitability of the center of the wandering nerve, as it activates the intestinal motility. Ponos, contributing to the liberation of the organism from non-visible or toxic substances, are protective. But with long-term diarrhea, deep disorders of digestion occur, associated with a violation of the secretion of intestinal juice, digestion and suction of food substances in the intestine. The slowdown in the peristalsis of the small intestine refers to the rare pathophysiological mechanisms for the formation of diseases. At the same time, the promotion of food casher in the intestines is inhibited and constipation develops. This clinical syndrome is usually a consequence of the pathology of the colon.

Chapter 10. Digestive System

Chapter 10. Digestive System

A brief overview of the functioning of the digestive system

Food products that we consume cannot be learned in this form. To start, food should be machined, translated into aqueous solution and cleaved chemically. Unused residues need to withdraw from the body. Since our gastrointestinal tract consists of the same components as food, its inner surface must be protected from the effects of digestive enzymes. Since we take food more often than it is digested and splitting products are absorbed, and in addition, the shag is eliminated once a day, in the gastrointestinal tract there should be an opportunity for food storage within a certain time. Coordination of all these processes is carried out primarily: (1) autonomous or gastroenterical (internal) nervous system (nervous plexus of the gastrointestinal tract); (2) Sounds come from the outside of the vegetative nervous system and visceral afferents, as well as (3) with numerous hormones of the gastrointestinal tract.

Finally, the thin epithelium of the digestive tube is a giant gate through which the pathogens of disease can penetrate into the body. There are a number of specific and nonspecific mechanisms for the protection of this border between the external environment and the inner world of the body.

In the gastrointestinal tract, the liquid internal environment of the body and the outer medium are separated from each other only very thin (20-40 microns), but huge in the area of \u200b\u200bthe epithelium layer (about 10 m 2), through which the substance necessary for the body can be absorbed.

The gastrointestinal tract consists of the following departments: mouth, throat, esophagus, stomach, delicate intestines, fat intestines, straight intestine and anus. Numerous exocrine glands are attached to them: salivary glands

oral cavity, ebner gland, gastric glands, pancreas, bile liver system and thin and large intestinal crypts.

Motor activityincludes chewing in the mouth, swallowing (pharynx and esophagus), grinding and mixing food with gastric juicy In the distal stomach, stirring (mouth, stomach, delicate intestine) with digestive juices, movement in all parts of the ventricular tract and temporary storage (proximal diversity of the stomach, blind intestine, ascending part of the colon, straight intestine). The time of food for each of the sections of the gastrointestinal tract is represented in Fig. 10-1. Secretionoccurs along the entire length of the digestive tract. On the one hand, secrets serve as lubricating and protective films, and on the other hand, contain enzymes and other substances that provide digestion. Secrecy implies the transport of salts and water from the interventicium into the clearance of the gastrointestinal tract, as well as the synthesis of proteins in the secretory cells of the epithelium and their transport through the apical (luminal) plasma membrane into the lumen of the digestive tube. Although secretion and can occur spontaneously, most of the iron tissue is under the control of the nervous system and hormones.

Digestion(Enzymatic hydrolysis of proteins, fats and carbohydrates), which is happening in the mouth, stomach and the small intestine is one of the main functions of the digestive tract. It is based on the work of enzymes.

Reabsorption(or in Russian suction)it implies the transport of salts, water and organic substances (for example, glucose and amino acids from the lumen of the gastrointestinal tract in blood). In contrast to secretion, the dimensions of reabsorption are determined rather, the proposal of reabsorbable substances. Reabsorption is limited to certain areas of the digestive tract: the delicate intestine (nutrients, ions and water) and the thick intestine (ions and water).

Fig. 10-1. Gastrointestinal tract: the overall structure of the structure and the time of passage.

Food is processed mechanically, stirred with digestive juices and is cleaving chemically. Splitting products, as well as water, electrolytes, vitamins and trace elements are reabsorbed. The glands allocate mucus, enzymes, H + and HCO 3 ions -. The liver supplies bile required to digest fats, and also contains products to be removed from the body. In all departments of the gastrointestinal tract, the contents in the proximal and distal direction occurs, while intermediate storage locations make possible discrete meals and emptying of the intestinal tract. Emptying time has individual features and depends primarily from the composition of food

Functions and composition saliva

Salus is formed in three large paired salivary glands: nearby (Glandula Parotis),submandibular (Glandula submandiBularis)and sublard (Glandula sublingualis).In addition, glazing glazed glances, chicks, chicks and pharynesses. Serous fluid is also distinguished ebnery glands located at the base of the language.

First of all, saliva is necessary for the feeling of flavoring incentives, for sucking (in newborns), for the oral hygiene and for wetting solid slices of food (when preparing them to swallow). The digestive enzymes of saliva are needed, in addition, to remove food residues from the oral cavity.

Functionsslyons of man are as follows: (1) solventfor nutrients, which only in dissolved form can be perceived by taste receptors. In addition, saliva contains mucins - lubricants- which facilitate chewing and swallowing solid food particles. (2) moisturizes the mouth cavity and prevents the spread of infections pathogens, due to the content lizozyme, Peroxidase and Immunoglobulin A (IGA),those. Substances with nonspecific or, in cases of IGA, specific antibacterial and antiviral properties. (3) contains digestive enzymes.(4) contains various growth factors,such as NGF. Nerve Growth Factorand EGF. (Epidermal Growth Factor).(5) Babies saliva needed for tight suction of lips to the nipple.

It has a slightly alkaline reaction. Osmolar saliva depends on the speed of the flow of saliva by the ducts of the salivary glands (Fig. 10-2 a).

Salus is formed in two stages (Fig. 10-2 b). First, the slices of the salivary glands are produced by isotonic primary saliva, which is secondally modified during the passage of gland output. Na + and Cl - reabsorbed, and K + and bicarbonate secreted. It is usually reabsorbing more ions than it is released, therefore the saliva becomes hypotonic.

Primary Slyunaarises as a result of secretion. In most salivary glands the protein-carrier providing the transfer to the Na + -K + -2Cl cell - (Cotransport),built into basolateral memb

wound of acinus cells. With this protein reader, the secondary accumulation is provided in the CL ion cell - which then passively go into the lumen of the gland ducts.

On the second stagein the output ducts from saliva nA + and CL are rebupping.Since the duct epithelium is relatively impenetrable for water, saliva becomes in it hypotonic.At the same time (small quantities) K + and HCO 3 - stand outdriver's epithelium in his lumen. Compared to blood plasma, saliva poor ions Na + and Cl -, but rich in ions K + and HCO 3 -. With a high speed of the flow of saliva, the transport mechanisms of the outputs do not cope with the load, therefore the concentration of K + falls, and NaCl increases (Fig. 10-2). The HCO 3 concentration is practically independent of the flow rate of the saliva by the gonducts.

Salyun enzymes - (1)α -amylase(also called birdin). This enzyme is distinguished almost exclusively by the parole salivary gland. (2) Nonspecific lipaseswhich are highlighted by Ebner's glands, located at the base of the language, especially important for the baby, as they can digest milk fat already in the stomach thanks to the enzyme of saliva, swallowed simultaneously with milk.

Selection of saliva is adjusted exclusively the CNS.Its stimulation is provided reflexunder the influence smell and taste of food.All large human salivary glands are innervized as sympatheticso I. parasympatheticnervous system. Depending on the quantities of mediators, acetylcholine (M 1 -Holinoreceptors) and norepinephorine (β 2 -adrenoreceptors), the composition of saliva changes near the oscinus cells. In hummist, the sympathetic fibers cause the secretion of more ductal saliva, poor water than when stimulated parasympathetic system. The physiological meaning of such dual innervation, as well as differences in the composition of saliva, are not yet known. Acetylcholine In addition, it causes (through M 3 -cholinoreceptors) reduction moepithelial cellsaround the acinus (Fig. 10-2 c), as a result of which the content of the acinus is extruded in the duct. Also acetylcholine contributes to the formation of kallipelines that release bradykinfrom KININOGEN blood plasma. Bradyikinin has a vasodilatory action. The extension of the vessels enhances the selection of saliva.

Fig. 10-2. Saliva and her education.

AND- Osmolayality and the composition of saliva depend on the rate of saliva. B.- Two stages of saliva formation. IN- Mioepithelial cells in salivary gland. It can be assumed that myoepithelial cells protect slices from expansion and rupture, which can be extended to high pressure in them as a result of secretion. In the duct system, they can perform a function aimed at reducing or expanding the lumen of the duct

Stomach

Stomach wall,the shown on its cut (Fig. 10-3 b) is formed by four shells: mucosa, submucosal, muscle, serous. Mucous membraneforms longitudinal folds and consists of three layers: epithelial layer, own plate, muscular plate. Consider all the shells and layers.

Epithelial mucosa layerpresented with single-layer cylindrical iron epithelium. It is formed by ferrous epitheliocytes - mucocytes secreting mucus. The mucus forms a continuous layer with a thickness of up to 0.5 microns, being an important factor in the protection of the gastric mucosa.

Owl plate mucous membraneformed by loose fiber junction tissue. It contains small blood and lymphatic vessels, nervous trunks, lymphoid nodes. The main structures of their own plates are glands.

Muscular mucosa plateit consists of three layers of smooth muscle tissue: internal and external circular; Middle longitudinal.

Sublifting shellit is formed by loose fibrous unformed connective tissue, contains arterial and venous plexus, ganglia of the submembraty nervous plexus of the Maisner. In some cases, large lymphoid follicles can be located here.

Muscular shellit is formed by three layers of smooth muscle tissue: internal oblique, medium circular, external longitudinal. In the pylorial stomach department, the circular layer reaches maximum development, forming a pyloric sphincter.

Serous shellit is formed by two layers: layer of loose fibrous unformed connective tissue and mesothelium lying on it.

All glands of the stomach,which are the main structures of their own plate - simple tubular glands.They open in gastric fossa and consist of three parts: dNA, body and shays (Fig. 10-3 c). Depending on localization glands are dividedon cardial, main(or foundal)and piloric.Building I. cellular composition These glands are unequal. Quantitatively prevail main glands.They are the most weak-resulted from all glands of the stomach. In fig. 10-3 B shows a simple tubular iron of the gastric body. The cell composition of these glands includes (1) surface epithelial cells, (2) cervical mucous cells (or additional), (3) regenerative cells,

(4) Parietal cells (or shelling cells),

(5) Main cells and (6) endocrine cells. Thus, the main surface of the stomach is covered with a single-layer high breeding epithelium, which is interrupted by numerous pits - in places of ducts stomach glands(Fig. 10-3 b).

Arteriespass through serous and muscular shells, giving them small branches, disintegrating to the capillaries. Main trunks form plexuses. The most powerful plexus is sublimated. From it, small arteries are deployed in their own plate, where the mucous plexus form. From the latter, capillaries, swelling glands and feeding epithelium departs. Capillaries merge into large star veins. Viennes form the plexus of the mucous membrane, and then the sublimated venous plexus

(Fig. 10-3 b).

Lymphatic systemthe stomach originates from blindly starting right under the epithelium and around the glance of the mucous membrane. Capillaries merge into the submembratus lymphatic plexus. The lymphatic vessels from it are muscular shell, taking into account the vessels of the lying between the muscular layers of the plexuses.

Fig. 10-3. Anatomical and functional stomach departments.

AND- Functionally stomach divided into a proximal department (tonic reduction: food storage function) and a distal department (mixing and processing function). Peristaltic waves of the distal stomach station begin in the area of \u200b\u200bthe stomach containing smooth muscles cells, the membrane potential of which fluctuates with the highest frequency. Cells of this area are drivers of the rhythm of the stomach. The scheme of the anatomical structure of the stomach, to which the esophagus fit is presented in Fig. 10-3 A. The stomach includes several departments - the cardiac diversity of the stomach, the bottom of the stomach, the body of the stomach with a paisker zone, the antrheral diversity of the stomach, the gatekeeper. Then the duodenum begins. The stomach can also be divided into the proximal department of the stomach and the distal stomach department.B.- section of the wall of the stomach. IN- Tubular Iron Body Stomach

Cells of tubular gland stomach

In fig. 10-4 B shows the tubular iron of the body of the stomach, and on the insert (Fig. 10-4 a), its layers are made, designated on the panel. Fig. 10-4 B shows the cells included in the simple tubular gland body of the stomach. Among these cells, we pay attention to the main, playing a pronounced role in the physiology of the stomach. This is, above all, parietal cells, or chopping cells(Fig. 10-4 V). The main role of these cells is the release of hydrochloric acid.

Activated shepherd cellshighlighted large amounts of isotonic fluid, which contains hydrochloric acid at a concentration to 150 mmol; Activation is accompanied by pronounced morphological changes in the shell cells (Fig. 10-4 V). Weakly activated cell has a network of narrow, branched channelian(The diameter of the lumen is about 1 μm), which are opened in the glory clearance. In addition, in the cytoplasm layer, bordering the enumeration of the tube, there is a large number tubulovicul.In the membrane, the tubulosyculin is built K + / H + -Ath FAZand ionic K + -and CL - - Channels.With strong activation, the cells of the tubulosiculus are embedded in the membrane of the tubules. This significantly increases the surface of the drive membrane, and the transport proteins (K + / H + -ATFAZ) and ion channels for K + and Cl - (Fig. 10-4 g) are embedded in it. With a decrease in the level of activation of the cell, the tobulosicular membrane is cleaved by the tubular membrane and persists in vesicles.

The HCL-secretion mechanism itself is unusual (Fig. 10-4 g), since it is carried out by H + - (and K +) - transporting ATFase in luminal (by the channel) membrane, and not as it is often found throughout the body - with using Na + / K + -ATFases of the basolateral membrane. Na + / K + -AT files of the shell cells ensures constancy interior environment Cells: In particular, contributes to the cell accumulation of K +.

Salonic acid is neutralized, so-called antacids. In addition, the secretion of HCl can be braked due to the blockade of Ranitidine H 2 -receptors (Histamine 2 -Receptors)clamps or braking activity H + / K + -ATFAZ omeprazole.

Main cellsendopepidases are isolated. Pepsin - proteolytic enzyme - stands out by the main cells of the human stomach gland in inactive form (pepsinogen).The activation of pepsinogen is carried out autocatalytically: first from the pepsinogen molecule in the presence of hydrochloric acid (pH<3) отщепляется пептидная цепочка длиной около 45 аминокислот и образуется активный пепсин, который способствует активации других молекул. Активация пепсиногена поддерживает стимуляцию обкладочных клеток, выделяющих HCl. Встречающийся в желудочном соке маленького ребенка gastricin (\u003d Pepsin C)correspond to labanman(Himosin, Renine) calf. It breaks down a certain molecular connection between phenylalanine and methioninone (Phet-Met-Communication) in casinogen(soluble milk protein), due to which this protein turns into an insoluble, but better digestible casein ("coagulation" of milk).

Fig. 10-4. The cellular structure of the simple tubular gland body of the stomach and the functions of the main cells that determine its structure.

AND- Tubular iron body of the stomach. Usually 5-7 such glands are poured into the hole on the surface of the stomach mucosa.B.- Cells included in the simple tubular gland body of the stomach. IN- Clamps in peace (1) and when activated (2). G.- secretion HCl by clad cells. In the secretion of HCl, two components can be detected: the first component (not subject to stimulation) is associated with the activity of Na + / K + -ATPhase localized in the basolateral membrane; The second component (prone to stimulation) is provided by H + / K + -ATPAZ. 1. Na + / K + -atfase maintains a high concentration of ions to + in the cell, which can exit cells through the channels into the stomach cavity. At the same time, Na + / K + -ATPAZ contributes to the removal of Na + from a cell, which accumulates in a cell as a result of a carrier protein, providing an exchange of Na + / H + (antiport) by the mechanism of secondary active transport. On each derived ion H + in the cell, one OH-ion remains, which interacts with CO 2 with the formation of HCO 3 -. The catalyst for this reaction is carboangeerase. HCO 3 - comes out of the cage through the basolateral membrane in exchange for CL -, which is then secreted into the cavity of the stomach (through the Cl --channels of the apical membrane). 2. At the luminal membrane H + / K + -ATFAZ provides the exchange of ions to + on H + ions, which go into the cavity of the stomach, which is enriched with HCl. On each dedicated Ion H + and in this case, from the opposite side (through the base membrane), the cell is leaving the HCO 3 anion 3 -. The ions K + are accumulated in the cell, go into the cavity of the stomach through K +-channels of the apical membrane, and then fall into the cell as a result of the operation of H + / K + -ATFases (circulation to + through the apical membrane)

Protection against self-equiping stomach wall

The integrity of the epithelium of the stomach primarily threatens the proteolytic effect of pepsin in the presence of hydrochloric acid. From such self-relocation stomach protects thick layer of tight mucuswhich is highlighted by the epithelium of the stomach walls, the addition cells of the bottom and body of the stomach, as well as cardiac and pylorarium glands (Fig. 10-5 A). Although pepsin and can split mucines of mucus in the presence of hydrochloric acid, mostly it is limited to the upper mucus layer, since deeper layers contain bicarbonate,which

rye is isolated by cells of the epithelium and contributes to the neutralization of hydrochloric acid. Thus, through the mucus layer, there is an H + -Gradient: from more acidic in the cavity of the stomach to alkaline on the surface of the epithelium (Fig. 10-5 b).

Damage to the epithelium of the stomach does not necessarily lead to serious consequences, provided that the defect will be quickly eliminated. In fact, such damage to the epithelium occur quite often; However, they are quickly eliminated due to the fact that neighboring cells are molded, migrate in the side direction and closed the defect. Following this, new cells are embedded as a result of mitotic division.

Fig. 10-5. Self-defense of the stomach wall from digestion due to secretion of mucus and bicarbonate

Structure of the wall of the small intestine

Small intestineconsists of three departments - duodenal, skinny and iliac guts.

The wall of the subtle intestines consists of various layers (Fig. 10-6). In general, outside under serous sheathpasses exterior muscle shell,which consists of outdoor longitudinal muscular layerand inner annular muscular layer,and the most inner is muscle plate mucous membrane,which separates submucose layerfrom mukozny. beams gAP Junctions)

The muscles of the outer layer of longitudinal muscles ensure the reduction of the intestinal wall. As a result, the intestinal wall is shifted relative to Hamus (food casher), which contributes to the best mixing of the chimus with digestive juices. Ring muscles narrows the intestinal lumen, and the muscle plate of the mucous membrane Lamina Muscularis Mucosae)provides the movement of villi. The nervous system of the gastrointestinal tract (gastroenterological nervous system) form two nervous plexuses: intermuscular nervous plexus and submucous nervous plexus. The CNS is able to influence the operation of the nervous system of the gastrointestinal tract through the sympathetic and parasympathetic nerves, which are suitable for the nervous plexus of the food tube. In the nervous plexuses begin afferent visceral fibers, which

pass nervous pulses in the central nervous system. (This wall device is also observed in the esophagus, stomach, a thick intestine and the rectum). To accelerate reabsorption, the surface of the small intestine mucous membrane is increased due to folds, porcelines and brush cuts.

The inner surface of the small intestine has a typical relief due to the presence of a number of formations - circular folds Kerkringa, Villageand crypt(Libekyun's intestinal glands). These structures increase the total surface of the small intestine, which contributes to the performance of its basic functions of digestion. Intestinal patches and crypts are the main structural-functional units of the mucous membrane of the small intestine.

Mucous(or mukoznaya shell)consists of three layers - epithelial, own plate and muscle plate mucosa (Fig. 10-6 a). The epithelial layer is represented by a single-layer cylindrical cut-off epithelium. In vile and crypts, it is represented by different types of cells. Epithelium Villagecompiled by four types of cells - main cells, glazing cells, endocrine cellsand paren cells.Epithelium Crypt.- Five species

(Fig. 10-6 V, d).

In the cavertes enterocyte

Boxed enterocytes

Fig. 10-6. The structure of the wall of the small intestine.

AND- The structure of the duodenum. B.- The structure of a large duodenal duodenum:

1. Large duodenal nipples. 2. Ampoule duct. 3. Sphinters of ducts. 4. Pancreatic duct. 5. Common bull duct. IN - The structure of various departments of the small intestine: 6. The glands of the duodenum (brunner gland). 7. Serous shell. 8. The outer longitudinal and internal circular layers of the muscular shell. 9. Subliminate base. 10. The mucous membrane.

11. Private plate mucous membrane with smooth muscle cells. 12. Group lymphoid nodules (lymphoid plaques, peer plaque). 13. Vile. 14. Folds. G. - Structure of the wall of the small intestine: 15. VILLINE. 16. Circular fold.D. - Vile and crypts of the mucous membrane of the small intestine: 17. The mucous membrane. 18. Own plate mucous membrane with smooth muscle cells. 19. Sublifting base. 20. The outer longitudinal and internal circular layers of the muscular shell. 21. Serous shell. 22. Vile. 23. Central Milky Sinus. 24. Single lymphoid nodule. 25. Intestinal iron (Iron Liborkunova). 26. Lymphatic vessel. 27. Sublifting nervous plexus. 28. The internal circular layer of the muscular shell. 29. Muscular nervous plexus. 30. The outer longitudinal layer of the muscular shell. 31. Artery (red) and vein (blue) of the sublifted layer

Functional morphology of the mucous membrane of the small intestine

The three divisions of the small intestine have the following differences: the duodenum has large nipples - duodenal glands, the height of the villium, which increases from the duodenum to the ilium, is differently width (wider - in the duodenum), and the quantity (the largest amount in the duodenum ). These differences are shown in Fig. 10-7 B. Further, there are group lymphoid follicles in the iliac (smelting). But they can sometimes be discovered in a duodenalist.

Vile- Palpid protrusion of the mucous membrane in the intestinal lumen. They contain blood and lymphatic capillaries. Vile is able to actively shrink due to the components of the muscular plate. This contributes to the suction of chimus (pumping function of the VILDIN).

Folding Kerkringa(Fig. 10-7 g) are formed by protruding the mucous membranes and submucosal shells into the intestinal lumen.

Crypta- This is the recesses of the epithelium into the sowing plate of the mucous. They are often regarded as glands (Libekyun glands) (Fig. 10-7 V).

The delicious intestine is the main place of digestion and reabsorption. Most enzymes encountered in the lumen of the intestines are synthesized in the pancreas. The delicate intestine itself highlights about 3 liters with rich liquid mucins.

For the intestinal mucosa, the presence of intestinal villos (Villi Intestinalis),which increase the surface of the mucous membrane is 7-14 times. Epithelium Village goes to Libekyun's secretory crypts. Crypts lie at the base of the Village and open in the direction of the intestinal lumen. Finally, each epithelial cell on the apical membrane carries the brush cut (microvascular), which

paradise increases the surface of the intestinal mucosa of 15-40 times.

Mitotic division occurs in the depths of Crypt; Daughter cells migrate to the top of the villus. All cells, with the exception of PAnet cells (providing antibacterial protection), take part in this migration. The whole epithelium is completely updated within 5-6 days.

Epithelium of the small intestine is covered a layer of gel mucus,which is formed by glass-like crypt and villi cells. When the gatekeeper sphincter opens, the yield of chimus in the duodenum launches increased secretion of mucus iron Brunner.Himus transition to the duodenum causes the garbage in the blood secretinaand cholecystokinin. Secretin launches in the pancreatic duct epithelium secretion of alkaline juice, which is also needed to protect the mucous membrane of the duodenum from the aggressive stomach juice.

About 95% of the Village epithelium are occupied by the chibsal main cells. Although their main task is reabsorption, they are the most important sources of digestive enzymes that are localized either in the cytoplasm (amino and dipeptidases) or in the brush cut membrane: lactase, sacrase-isomaltase, amino and endopeptidase. These brush kaimki enzymesthey are integral proteins of the membrane, and part of their polypeptide chain together with the catalytic center is directed to the intestinal lumen, so enzymes can be hydrolyolized in the cavity of the digestive tube. Their secretion in the clearance in this case is not necessary (wear digestion). Cytosolic enzymesthe epithelial cells take part in the digestion processes when they split the reabsorbed cell of the protein (intracellular digestion), or when the epithelium cells containing their cells are dying, they will be discouted into the lumen and are destroyed, highlighting enzymes (band digestion).

Fig. 10-7. Histology of various departments of the small intestine - duodenal, skinny and iliac guts.

AND- Pork and crypts of the mucous membrane of the small intestine: 1. mucous membrane. 2. Own plate mucous membrane with smooth muscle cells. 3. Subliminate base. 4. External longitudinal and internal circular layers of muscle shell. 5. Serous shell. 6. VILLIN. 7. Central Milky Sinus. 8. Single lymphoid nodule. 9. Intestinal iron (Iron Liborkunova). 10. Lymphatic vessel. 11. Sublifting nervous plexus. 12. Internal circular layer of muscle shell. 13. Muscular nervous plexus. 14. The outer longitudinal layer of the muscular shell.

15. Artery (red) and vein (blue) of the sublifted layer.B, B. - the structure of the VILLIN:

16. Box and shaped cell (single-cell iron). 17. Prismatic epithelium cells. 18. Nervous fiber. 19. Central Milky Sinus. 20. Microhemacircraft breeder of VILLIN, a network of blood capillaries. 21. Own plate mucous membrane. 22. Lymphatic vessel. 23. Venula. 24. Arteriol.

Small intestine

Mucous(or mukoznaya shell)it consists of three layers - the epithelial, own plate and the muscle plate of the mucous membrane (Fig. 10-8). The epithelial layer is represented by a single-layer cylindrical cut-off epithelium. The epithelium contains five major cell populations: columnar epitheliocytes, glass-like exocrinocytes, PAnet cells, or exocrinocytes with acidophilic granules, endocrinocytes or K-cells (Kulchitsky cells), as well as m-cells (with microslites), which are modifications of column epithelocytes.

Epithelines are covered vileand adjacent to them crypts.It consists of a majority of reabsorbing cells, which in the luminal membrane carry brush cut. Balo-shaped cells forming mucus, as well as pan-cell cells and various endocrine cells are scattered. The cells of the epithelium are formed as a result of the division of the crypt epithelium,

from where they migrate 1-2 days in the direction of the tip of the Vile and are discarded there.

In vile and crypts, it is represented by different types of cells. Epithelium Villagecompiled by four cell types - main cells, glassoid cells, endocrine cells and PAnet cells. Epithelium Crypt.- Five species.

The main type of cells of the epithelium Village - carable enterocytes. In the cavertes enterocyte

the epithelium of the membrane villine forms microvills coated with glycocalix, and it adsorbs the enzymes involved in the trim digestion. Due to the microvascular, the suction surface increases 40 times.

M-cells(cells with microscopes) are a kind of enterocytes.

Boxed enterocytespork epithelium is unicellular mucous glands. They produce carbohydrate-protein complexes - mucins that perform a protective function and promoting the promotion of components of food in the intestine.

Fig. 10-8. Morphogistological structure of VILFI and crypts of the small intestine

Colon

Colonit consists of mucosa, submucosal, muscular and serous shells.

The mucous membrane forms the terrain of colon - folds and crypts. There are no vile in the colon. Single-layer cylindrical mucous membrane epithelium, and contains the same cells as the epithelium crypt of the small intestine - carbon, glass-shaped endocrine, monscable, patenet cells (Fig. 10-9).

The submucous shell is formed by loose fibrous connective tissue.

Muscular shell has two layers. The inner circular layer and the outer longitudinal layer. The longitudinal layer is not solid, but forms

three longitudinal tapes. They are shorter and therefore the intestine is collected in the "harmonic".

The serous shell consists of loose fibrous connective tissue and mesothelium and has a protrusion containing fatty tissue.

The main differences of the walls of the colon (Fig. 10-9) from fine (Fig. 10-8) is: 1) the absence in the relief of the mucous membrane of the Village. Moreover, the crypts are greater than in the small intestine, depth; 2) the presence in the epithelium of a large number of glazing cells and lymphocytes; 3) the presence of a large number of single lymphoid nodules and the absence of peyer plaques in its own plate; 4) the longitudinal layer is not solid, but forms three tapes; 5) the presence of protrusion; 6) The presence of fatty letters in the serous shell.

Fig. 10-9. Morphogistological structure of a large intestine

Electric activity of muscular cells of the stomach and intestines

Smooth intestinal musculature consists of small, spine-shaped cells forming beamsand forming cross-links with adjacent beams. Inside one bundle, the cell is connected to each other both mechanically and electrically. Thanks to such electrical contacts, the action potentials are distributed (through the intercellular slot contacts: gAP Junctions)for the entire bundle (and not only on separate muscle cells).

For muscle cells of the anthral ventricular and intestines and intestines are usually characterized by rhythmic oscillations of membrane potential (Slow Waves)amplitude 10-20 mV and a frequency of 3-15 / min (Fig. 10-10). At the moment of slow waves, muscle bundles are partially reduced, so the wall of these departments of the gastrointestinal tract is in the tone; This happens in the absence of potentials of action. When the membrane potential reaches the threshold and exceeds it, the action of the action potentials follows with a small interval after each other (Speakers sequence).The generation of potentials of action is due to Ca 2+th (Ca 2+-channels L-type). Increasing Ca 2+ concentration in cytosol launches fazic cuts,which are especially pronounced in the distal stomach department. If the magnitude of the diaphragmal potential of rest is approaching the value of the threshold potential (but does not reach it; the membrane rest potential is shifted towards depolarization), then the potential of slow oscillations begins

regularly exceed the threshold value of the potential. In this case, there is a frequency in the occurrence of spike sequences. Smooth muscles is reduced every time the sequence of spikes is generated. The frequency of rhythmic cuts corresponds to the frequency of slow oscillations of the membrane potential. If the membrane potential of resting the cells of smooth muscles is even more approaching the threshold potential, then the duration of spike sequences increases. Develops spasmsmooth muscles. If the membrane resting potential is shifted towards more negative values \u200b\u200b(towards hyperpolarization), then the spike activity is terminated, and rhythmic reductions are stopped with it. If the membrane hyperpolarizes even more, then the amplitude of slow waves and muscle tone is reduced, which in the end leads to paralysis of smooth muscles (atony).Due to what ion currents there are oscillations of the membrane potential, it is not yet clear; Obviously one thing is that the nervous system does not affect the fluctuations in the membrane potential. The cells of each bunch of muscles have one, only by them with the characteristic frequency of slow waves. Since adjacent beams are connected to each other by electrical intercellular contacts, the beam with a higher frequency of waves (Rhythm driver)it will impose this frequency to the adjacent beam with a lower frequency. Tonic reduction of smooth musclesfor example, the proximal stomach department is due to the opening of Ca 2+ - channels of another type, which are chemide-dependent, and not potentially dependent.

Fig. 10-10. The membrane potential of the cells of the smooth muscles of the gastrointestinal tract.

1. As long as the wave-like cells of the membrane potential of a smooth muscles (oscillation frequency: 10 min -1) remains below the value of the threshold potential (40 mV), the potentials of the action (spikes) are missing. 2. When (for example, stretching or acetylcholine) depolarization, the spike sequence is generated each time the peak of the membrane potential wave exceeds the value of the threshold potential. For such sequences, spikes are followed by rhythmic reductions in smooth muscles. 3. Speakers are generated continuously if the minimum values \u200b\u200bof the oscillations of the membrane potential lie above the threshold value. A long reduction is developing. 4. Potentials of the action are not generated with strong shears of the membrane potential towards depolarization. 5. Hyperpolarization of the membrane potential causes attenuation of slow potential fluctuations, and smooth muscles completely relaxes: Athonia

Reflexes of the gastroenterological nervous system

Part of the reflexes of the gastrointestinal tract is its own gastroenteroral (local) reflexes,in which the sensory sensitive afferent neuron activates the nervous plexus cell innervating the smooth muscle cells located next to it. The impact on smooth muscle cells may be exciting or braking depending on which type of plexus neuron turns out to be activated (Fig. 10-11 2, 3). The implementation of other reflexes involves motor neurons located proximal or distal than the place of stimulation. For peristaltic reflex(for example, as a result of stretching the wall of the digestive tube), touch neurons are excited.

(Fig. 10-11 1), which, through the brake interneurone, has a braking effect on the longitudinal muscles of the digestive tube departments lying for a proximalous, and a discharging effect on the annular muscles (Fig. 10-11 4). At the same time, a longitudinal musculature is activated through the exciting interneagon (the food tube is shortened), and the annular muscles relaxes (Fig. 10-11 5). With a peristaltic reflex, a complex series of motor events is launched, caused by stretching of the muscular wall of the digestive tube (for example, esophagus; Fig. 10-11).

The movement of food lumps shifts the place of activation of the reflex distal, which again moves the food lump, the result of which is almost continuous transport in the distal direction.

Fig. 10-11. Reflex arc reflexes gastroenterological nervous system.

The excitation of the afferent neuron (light green) due to the chemical or, as shown in the picture (1), the mechanical stimulus (stretching the wall of the food tube due to the edible lump) activates in the simplest case only one excitable (2) or only one brake engine or secretory Neuron (3). Reflexes of the gastroenterological nervous system are still usually in more complex switching schemes. With a peristaltic reflex, for example, neuron, which is excited during tension (light green), excites in the ascending direction (4) the brake interneurone (purple), which in turn slows down the exciting motoryneron (dark green), innervating longitudinal muscles, and removes braking with Brake motor mechanone (red) ring musculature (abbreviation). At the same time in the descending direction (5), an exciting interneurone (blue) is activated, which through exciting or, accordingly, braking motionones in the lying distal part of the intestine causes a reduction in the longitudinal muscles and relaxation of ring muscles.

Parasympathetic innervation of the gastrointestinal tract

The innervation of the gastrointestinal tract is carried out using the vegetative nervous system (parasympathetic(Fig. 10-12) and sympatheticinnervation - efferent nerves), as well as visceral afferents(afferent innervation). Parasympathetic proteggalionic fibers, innervating most of the digestive tract, come in the composition of wandering nerves (N. Vagus)from the oblong brain and in the composition of the pelvic nerves (NN. Pelvici)from the sacrilant spinal cord. The parasympathetic system sends fibers to exciting (cholinergic) and brake (peptidergic) cells of intermushkin nervous plexus. Preggling sympathetic fibers begin from cells lying in the side horns of the sternum-lumbar spinal cord. Their axons innervate the intestinal blood vessels or suitable to the cells of nerve plexuses, having a braking effect on their exciting neurons. Visceral afferents starting in the wall of the gastrointestinal tract are held as part of wandering nerves (N. Vagus),in the composition of atruman nerves (NN. Splanchnici)and pelvic nerves (NN. Pelvici)to the oblong brain, sympathetic ganglia and to the spinal cord. With the participation of sympathetic and parasympathetic nerve systems, many reflexes of the gastrointestinal tract proceeds, including the expansion reflex during filling and the intestinal paresis.

Although the reflex acts carried out by the nerve plexuses of the gastrointestinal, the tract may proceed independently of the influence of the central nervous system (CNS), but they are under the control of the CNS, which ensures certain advantages: (1) the part of the digestive tract can be quickly exchanged. information via CNS and thereby coordinate their own functions, (2) the functions of the digestive tract can be subject to more important interests of the body, (3) information from the ventricular tract can be integrated at different levels of the brain; What, for example, in the case of abdominal pain, may even cause conscious sensations.

The innervation of the gastrointestinal tract is provided by vegetative nerves: parasympathetic and sympathetic fibers and, moreover, afferent fibers, so-called visceral afferets.

Parasymaptic nervesthe gastrointestinal tract overlook the two independent sections of the CNS (Fig. 10-12). Nerves serving the esophagus, stomach, the small intestine and the rising hatch (as well as the pancreas, gallbladder and the liver), originate from the neurons of the oblong brain (Medulla Oblongata)axons of which form a wandering nerve (N. Vagus),whereas the innervation of the remaining departments of the gastrointestinal tract begins with neurons the sacrum of the spinal cord,axons of which form pelvic nerves (NN. Pelvici).

Fig. 10-12. Parasympathetic innervation of the gastrointestinal tract

Effect of parasympathetic nervous system on muscle plexus neurons

In the entire digestive tract, parasympathetic fibers activate target cells through nicotine cholinergic receptors: one type of fibers forms synapses on cholinergic excitingand another type - on peptidergic (NCNA) brakenervous plexus cells (Fig. 10-13).

Axons of the pregganionic fibers of the parasympathetic nervous system are switched in intermushkin nerve plexus on exciting cholinergic or brake non-cholinergic-non-adrenergic (NCNA-Ergic) neurons. Postganglionic adrenergic neurons of the sympathetic system operate in most cases inhibitory on the neurons of the plexus, which stimulate motor and secretory activity.

Fig. 10-13. Innervation of the gastrointestinal tract in the vegetative nervous system

Sympathetic innervation of the gastrointestinal tract

Preggangionary cholinergic neurons sympathetic nervous systemlie in intermediolatoral pillars breast and lumbar spinal cord(Fig. 10-14). The axons of the neurons of the sympathetic nervous system come out of the thoracic spinal cord through the front

the roots and pass in the atrief nerves (NN. splanchnici)to upper cervical gangliaand K. perverter Ganglia.There is a switching to postganglyonary noradrenergic neurons, whose axons form synapses on the cholinergic excitatory cells of the intertensive plexus and through α receptors provide brakingimpact on these cells (see Fig. 10-13).

Fig. 10-14. Sympathetic innervation of the gastrointestinal tract

Affective innervation of the gastrointestinal tract

In the nerves that ensure the innervation of the gastrointestinal tract, in percentage more than the afferent fibers than the efferent. Ending sensory nervesare non-specialized receptors. One group of nerve endings is localized in the junction tissue of the mucous membrane near its muscle layer. It is assumed that they perform the function of chemoreceptors, but it is not yet clear which substances reabsorbed in the intestines activate these receptors. Perhaps the peptide hormone (Paraconnection) takes part in their activation. Another group of nerve endings lies inside the muscular layer and has the properties of mechanoreceptors. They react to mechanical changes that are associated with a reduction and stretching of the wall of the digestive tube. The afferent nerve fibers go from the gastrointestinal tract or as part of the nerves of a sympathetic or parasympathetic nervous system. Some afferent fibers coming in sympathetic

nerves form synapses in the prevertabral ganglia. Most of the afferents passes through pre- and paravertebral ganglia without switching (Fig. 10-15). Neurons of afferent fibers lie in sensitive

spinal gangles rear spinal cord roots,and their fibers are included in the spinal cord through the rear roots. The afferent fibers that pass in the composition of the wandering nerve form an afferent link the reflexes of the gastrointestinal tract occurring with the participation of the wandering parasympathetic nerve.These reflexes are especially important for the coordination of the motor function of the esophagus and the proximal department of the stomach. Sensitive neurons whose axons go in the wandering nerve, localized in Ganglion nodosum.They form connections with nuclear nucleus neurons (Tractus Solitarius).The information transmitted by them reaches the progenglyonary parasympathetic cells localized in the Dzoral Venus Nerva Core (Nucleus Dorsalis N. Vagi).Afferent fibers, which are used in the composition of pelvic nerves (NN. Pelvici),take part in the reflex of defecation.

Fig. 10-15. Short and long visceral afferents.

Long afferent fibers (green), the cells of the cells of which lie in the rear roots of the spinal ganglia, pass through the pre- and paravertebral ganglia without switching and fall into the spinal cord, where they either switch to the neurons of ascending or downstream paths, or in the same spinal cord segment Switched on the pregganionic vegetative neurons, as in the lateral intermediate gray matter (Substantia IntermedioLateralis) breast spinal cord. In short affairs, the reflex arc closes due to the fact that switching to the efferent sympathetic neurons is already carried out in sympathetic ganglia

The main mechanisms of transithelial secretion

The proteins-carriers built into the luminal and basolateral membrane, as well as the composition of the lipids of these membranes, determine the polarity of the epithelium. Perhaps the most important factor determining the polarity of the epithelium is the presence of the cells of the secreting epithelium cells in the basolateral membrane Na + / k + -atphases (Na + / K + - "pump"),sensitive to Obaine. Na + / K + -ATFase converts the chemical energy of ATP into electrochemical gradients Na + and K +, directed into a cell or from the cell, respectively (primary active transport).The energy of these gradients can be reused to transport other molecules and ions actively through the cell membrane against their electrochemical gradient. (Secondary Active Transport).This requires specialized transport proteins, so-called carrierswhich either provide simultaneous transfer of Na + into the cell along with other molecules or ions (cotransport) or exchange Na + on

other molecules or ions (antiport). The secretion of ions in the lumen of the digestive tube generates osmotic gradients, so water follows ions.

Active secretion of potassium

In the cells of the epithelium K + actively accumulates with the Na +-K +--Racuosos located in the basolateral membrane, and Na + rolls out from the cell (Fig. 10-16). In the epithelium, in which the secretion of K +, K + -Kanals are located in the same place where the pump is located (the secondary use of K + on the basolateral membrane, see Fig. 10-17 and Fig. 10-19). The simple mechanism of secretion K + can be ensured by embedding numerous to +-channels into a luminal membrane (instead of basolateral), i.e. In the epithelial cell membrane from the lumen of the digestive tube. In this case, the accumulated in the cell K + goes into the lumen of the digestive tube (passively; Fig. 10-16), and the anions are followed by K +, as a result of which the osmotic gradient occurs, so water is released into the lumen of the digestive tube.

Fig. 10-16. Transtephelial secretion KCL.

Na +./ K + -ATFAZ, localized in the baso-cell cell membrane, when used 1 mol ATP "pumps" from a cell 3 praying Na + ions and "pumps" into a cell 2 praying to +. While Na + enters the cage throughNa +.-Canals located in the basolateral membrane, K + yions leave the cage through K +-channels localized in the luminal membrane. As a result of moving to + through the epithelium, transverse potential in the lumen is set through the epithelium, as a result of which the CL ions are intercelled (through dense contacts between epithelial cells), they are also rushed into the lumen of the digestive tube. As stoichiometric values \u200b\u200bshow in the figure, 1 mol ATF is released 2 praying to +

TransPithelial secretion NaHCO 3

Most secreting epithelial cells first secrete an anion (for example, HCO 3 -). The driving force of this transport is an electrochemical Gradient Na +, directed from the extracellular space into a cell, which is established thanks to the mechanism of the primary active transport of the Na + -K -K--KOP operation. The potential energy of the Na + gradient is used by carrier proteins, and Na + is transferred through the cell membrane into the cell along with another ion or molecule (kittensport) or exchange to another ion or molecule (antiport).

For secretion HCO 3 -(for example, in pancreatic ducts, in the glands of Brunner or in bile ducts), Na + / N +-exchanger is needed in the baselateral cell membrane (Fig. 10-17). H + ions using secondary active transport are derived from the cell, as a result, it remains ions, which interact with CO 2 with the formation of NSO 3 -. The role of the catalyst in this process is carboangeezes. The resulting NSO 3 comes out of the cell in the direction of the lumen of the gastrointestinal tract or through the channel (Fig. 10-17), or with the help of a carrier protein operating C1 - / NSO 3. In all likelihood, both mechanisms are active in the pancreatic duct.

Fig. 10-17. The transithelial secretion of NaHCO 3 becomes possible when H + yions are actively displayed from the cell through the baselateral membrane. The protein-carrier is responsible for this, which, according to the mechanism of secondary active transport, ensures the transfer of H + ions. The driving force of this process is a Na + chemical gradient, supported by Na + / K + -At FAZ. (Unlike Fig. 10-16, the ions of K + entering the cell from the cell from the cell through the k +-channels of the Na + / K + -ATFases). On each ion H +, leaving the cell, one OH ion remains, which binds to CO 2, forming HCO 3. This reaction is catalyzed by carboangeyndase. HCO 3 - diffuses through the anionic channels into the lumen of the duct, which leads to the occurrence of transverseity potential, in which the contents of the lumen of the duct are negatively charged with respect to the interstiscum. Under the action of such transithelial potential, Na + ions through dense contacts between the cells are rushed into the lumen of the duct. Quantitative balance indicates that 1 mole of NaHCO 3 is spent 1 mol ATF

TransPithelial secretion NaCl

Most secreting epithelial cells first secrete an anion (for example, Cl -). The driving force of this transport is an electrochemical Gradient Na +, directed from the extracellular space into a cell, which is established thanks to the mechanism of the primary active transport of the Na + -K -K--KOP operation. The potential energy of the Na + gradient is used by carrier proteins, and Na + is transferred through the cell membrane into the cell along with another ion or molecule (cotransport) or exchanged to another ion or molecule (antiport).

A similar mechanism is responsible for the primary secretion of the Cl -, which provides the driving force of the process of secretion of the liquid in the terminal

the departments of the salivary gland gland, in the acynes of the pancreas, as well as in the tear glands. Instead of the Na + / H + exchanger in basoolateral membranethe epithelial cells of these organs are localized by a carrier providing a conjugate transfer of Na + -K + -2CL - (Cotransport;fig. 10-18). This carrier uses the Na + gradient for (secondary active) CL accumulation - in the cell. CL cells can passively extend through the ion channels of the luminal membrane into the lumen of the fiber of the gland. In this case, there is a negative transitaneal potential in the lumen of the duct, and Na + rushes into the lumen of the duct: in this case, through dense contacts between the cells (intercellular transport). The high concentration of NaCl in the lumen of the duct stimulates the water current along the osmotic gradient.

Fig. 10-18. A variant of transithelial secretion of NaCl, which requires the active accumulation of CL - in the cell. In the gastrointestinal tract, at least two mechanisms are responsible for this (see also Fig. 10-19), for one of which the carrier is localized in the basolateral membrane, which provides simultaneous transfer of Na + -2Cl - -k + through the membrane (Kotransport ). It works under the influence of a chemical gradient Na +, which, in turn, is supported by Na + / K + -Ath FAZ. K + ions fall into the cell both using the mechanism of the kittens and with Na + / k + -at phases and extend from the cell through the baselateral membrane, and CL - leaves the cell through the channels localized in the luminal membrane. The probability of their opening increases due to the Tsamf (subtle intestine) or cytosol Ca 2+ (terminal glands of glands, acinuses). There is a transithelial potential negative in the lumen of the duct, providing the intercellular secretion of Na +. Quantitative balance indicates that 1 mol ATF stands out 6 mole NaCl

TransPithelial secretion NaCl (option 2)

This, other secretion mechanism is observed in the cells of the acycous pancreatic gland, which

they have two carriers localized in the baselateral membrane and providing ionic exchanges Na + / H + and C1 - / NSO 3 - (antiport; Fig. 10-19).

Fig. 10-19. Option of transithelial secretion NaCl (see TAKE Fig. 10-18) which begins with the fact that with the help of basolateral Na + / H +-methods (as in Fig. 10-17), HCO 3 ions are accumulated in the cell. However, later, this HCO 3 - (unlike Fig. 10-17) leaves the cell using the CL--HCO 3 carrier - (antiport) located on the baselateral membrane. As a result of CL - as a result ("tertiary") active transport falls into the cage. Through Cl - -Kanals located in the luminal membrane, Cl - comes out of the cell in the lumen of the duct. As a result, there is a transverse potential in the lumen of the duct, at which the contents of the lumen of the duct carries a negative charge. Na + under the influence of transverseity potential rushes into the lumen of the duct. Energy balance: here 1 mol used ATF is released 3 mole NaCl, i.e. 2 times less than in the case of the mechanism described in Fig. 10-18 (DPC \u003d diphenylaminamicarboxylate; sits \u003d 4-acetamino-4 "-Isotiocyan-2.2" -Disulfonstilben)

Synthesis of secreted proteins in the gastrointestinal tract

Certain cells are synthesized proteins not only for their own needs, but also for secretion. The Matrix RNA (MRNA) for the synthesis of export proteins is not only information about the amino acid sequence of the protein, but also on the initial signal sequence of amino acids. The signal sequence ensures that protein is synthesized on the ribosome in the cavity of the rough endoplasmic reticulum (RER). After cleaving a signal sequence of amino acids, the protein falls into the Golgi complex and, finally, into condensing vacuoles and mature sparkling granules. If necessary, it is thrown out of the cell as a result of exocytosis.

The first stage of any synthesis of protein is the flow of amino acids in the base of the cell. With the help of aminoacyl-TRNA-synthetase, amino acids are attached to the corresponding transport RNA (TRNA), which delivers them to the place of protein synthesis. Protein synthesis

wills on ribosomeswhich "read" with matrix RNA information about the sequence of amino acids in protein (broadcast).mRNA for a protein intended for export (or for embedding in a cell membrane) is not only information about the sequence of amino acids of the peptide chain, but also connected at the initial MRNA information about amino acid signal sequence (signal peptide).The length of the signal peptide is about 20 amino acid residues. After the signal peptide is ready, it immediately binds to the cytosolic molecule recognizing the signal sequences - SRP.Signal Recognition Particle.SRP blocks protein synthesis until the entire ribosomal complex will be entrenched on SRP receptor(gentle protein) rough cytoplasmic reticulum (RER).After that, the synthesis begins again, while the protein is not released into cytosol and after the time it falls in the cavity Rer (Fig. 10-20). After the end of the broadcast, the signal peptide is cleaved by peptidase located in the RER membrane, and the new protein chain is ready.

Fig. 10-20. The synthesis of protein intended for export in the cell-cellular cell.

1. The ribosome is associated with the MRNA chain, and the end of the synthesized peptide chain begins to leave the ribosome. Amino acid signal sequence (signal peptide) protein intended for export binds to a molecule recognizing signal sequences (SRP, signal Recognition Particle). SRP blocks the position in the ribosome (section A) to which the TRNA with attached amino acid is suitable during protein synthesis. 2. As a result, the broadcast is suspended, and (3) SRP together with the ribosoma binds to the SRP receptor located on the membrane of the rough endoplasmic reticulum (RER), so that the end of the peptide chain is in (hypothetical) RER membrane. 4. SRP split 5. The broadcast can continue, and the peptide chain grows in the RER cavity: translocation

Secretion of proteins in the gastrointestinal tract

concentrate. Such vacuoles turn into mature secretory granules,which are collected in the luminal (apical) part of the cell (Fig. 10-21 a). From these granules, the protein is released into the extracellular space (for example, in the lumen of the acinus) due to the fact that the granules membrane merge with the cell membrane and at the same time breaks: exocytosis(Fig. 10-21 b). Exocytosis is a constantly current process, but the effect of the nervous system or humoral stimulation can accelerate it significantly.

Fig. 10-21. The secretion of a protein intended for exports in the cell-cellular cell.

AND- Typical exocrine secretting protein cellcontained in the basal part of the cell tightly packaged layers of rough endoplasmic reticulum (RER), on ribosomes of which exported proteins are synthesized (see Fig. 10-20). At the smooth ends of RER, vesicles are separated containing proteins that fall to cIS- Registration of the Machinery of the Golgie (post-transmission modification), from trans-areas of which condensing vacuoles are separated. Finally, with the apical side of the cells, numerous mature secretory granules are presented, which are ready for exocytosis (B panel). B.- The figure shows exocytosis. Three lower, surrounded by the membrane of vesicles (secretory granule; Panel a) are still free in cytosol, while vesicles on the left at the top adjacent to the inside of the plasma membrane. The membrane of vesicles on the right above has already merged with the plasma membrane, and the contents of the vesicles are poured into the lumen of the duct

Synthesized in the RER cavity protein is packaged in small vesicles, which are separated from RER. Veinsicles containing protein suitable golgi complexand merge with his membrane. In the complex of the Golgi Peptide is modified (post-translation modification),for example, Glycolized and leaves then the Golgi complex inside condensing vacuoles.They are modified in them again and

Regulation of the secretion process in the gastrointestinal tract

EXCRINE glands of the digestive tract lying outside the walls of the esophagus, the stomach and intestines are innervated by the effectants of both the sympathetic and parasympathetic nervous system. The glands in the wall of the digestive tube are innervated by the nerves of the submembratus plexus. Epithelium mucosa and embedded glands contain endocrine cells that release gastrin, cholecystokinin, secretine, GIP (Glucose-Dependent Insuli-Release Peptide)and histamine. After ejection into the blood, these substances are regulated and coordinated by motorcy, secretion and digestion in the gastrointestinal tract.

Many, perhaps, even all, secretory cells at rest are secreted in small amounts of fluid, salts and proteins. In contrast to the reabsorbing epithelium, in which the transport of substances depends on the Na + gradient, provided by the activity of Na + / K + -ATPAZ of the base base membrane, the level of secretion can be significantly increased if necessary. Stimulation secretioncan be carried out as nervous systemso I. gumoral.

In the entire gastrointestinal tract between epithelial cells, cells, synthesizing hormones are scattered. They release a number of signaling substances: some of which are transported to their target cells on the circulatory channel (endocrine action),others - Paragamons - act on neighboring cells (Paraconnection).Hormones affect not only cells participating in the process of secretion of various substances, but also on the smooth muscles of the gastrointestinal tract (stimulate its activity or inhibit). In addition, hormones can have a trophic or anti-parentic effect on the cells of the gastrointestinal tract.

Endocrine cellsthe gastrointestinal tract has a bottle shape, while the narrow part is equipped with microvills and is directed toward the intestinal lume (Fig. 10-22 a). In contrast to epithelial cells that provide transportation of substances, in the base oil membrane of endocrine cells, it is possible to detect granules with proteins that take part in the processes of transport in the cell and decarboxylation of amine precursors. Endocrine cells are synthesized including biologically active 5-hydroxytrifamin.Such

endocrine cells are called Apud (Amine Precursor Uptake and DecarBoxYlation)cells, since they all contain carriers needed to capture tryptophan (and histidine), and enzymes that ensure the decarboxylation of tryptophan (and histidine) to tripartamine (and histamine). In total, there are at least 20 signaling substances formed in the endocrine stomach and small intestine cells.

Gastrin,taken as an example, synthesized and released FROM(astrin.)-Lesters.Two thirds of the G-cells are in the epithelium, lining the anthral diversity of the stomach, and one third - in the mucous layer of the duodenum. Gastrin exists in two active forms G34.and G17(The numbers in the title indicate the number of amino acid residues constituting the molecule). Both forms differ from each other by the place of synthesis in the digestive tract and the biological age of the half-life. Biological activity of both forms of gastrin due to C-terminus peptide-Try-Met-ASP-PE (NH2). This sequence of amino acid residues is also contained in synthetic pentagastrine, Boc-β-Ala-Trymet-ASP-PHE (NH 2), which is introduced into the body to diagnose the secretory function of the stomach.

Incentive for releasegastrine in blood is primarily the presence of sprouting products of proteins in the stomach or in the lumen of the duodenum. Efferterent wandering nerve fibers also stimulate the release of gastrin. The fibers of the parasympathetic nervous system activate the G-cells are not directly, but through intermediate neurons that release GPR.(Gastrin-Release Peptide).The release of gastrin in the anthral stomach department is braked when the pH value of the gastric juice is reduced to the level of less than 3; Thus, a negative feedback loop occurs, with which the too strong or too long secretion of the gastric juice is stopped. On the one hand, the low pH right slows down G-cellsanthral stomach department, and on the other hand, stimulates D-cells,which release somatostatin (SIH).Subsequently, somatostatin has a brake effect on G-cells (Paraconnection). Another possibility for braking the secretion of gastrin is that the fibers of the wandering nerve can stimulate the secretion of somatostatin from D-cells through CGRP.(Calcitonin Gene-Related Peptide) -ergic interneurons (Fig. 10-22 b).

Fig. 10-22. Regulation of secretion.

AND- Endocrine cell of the gastrointestinal tract. B.- Regulation of the secretion of gastrin in the antral stomach department

Sodium reabsorption in a small intestine

The main departments where processes occur reabsorption(or in Russian terminology suction)in the gastrointestinal tract, are a skinny intestine, the ileum and the upper sequel. The specifics of the hectic intestine and the ileum lies in the fact that the surface of their luminal membrane is increased more than 100 times due to intestinal pranks and high brush cuts

Mechanisms with the help of which salts, water and nutrients are reabidated, are similar to kidney. Transportation of substances through the cells of the epithelium of the gastrointestinal tract depends on the activity of Na + / K + -atphase or H + / K + -atphase. Various embedding of carriers and ion channels into luminal and / or basolateral cell membrane determines which substance will be reabidated from the lumen of the digestive tube or secreted into it.

For a thin and large bowel, several suction mechanisms are known.

For the small intestine, the suction mechanisms presented in fig. 10-23 AI I.

fig. 10-23 V.

Mechanism 1.(Fig. 10-23 a) Localized primarily in the Torkychka. Na. + yions crossed the brush cut here using various carriers proteinswhich use the energy (electrochemical) gradient Na + to the cell, for reabsorption glucose, galactose, amino acids, phosphate, vitaminsand other substances, therefore, these substances fall into the cell as a result of (secondary) active transport (Cotransport).

Mechanism 2.(Fig. 10-23 b) inherent in the turntable and a busty bubble. It is based on the simultaneous localization of two carriersin the luminal membrane, providing ion exchanges Na + / H +and CL - / HCO 3 - (antiport),which allows you to reabsorb NaCl.

Fig. 10-23. Reabsorption (suction) Na + in the small intestine.

AND- Conjugated reabsorption Na +, Cl - and glucose in the small intestine (primarily in the Torkychka). The electrochemical gradient Na + is directed to the cage, which is supported by Na +/ K +. -ATFAZ, serves as a driving force for the luminary carrier (SGLT1), with which the mechanism of secondary active transport Na + and glucose is entered into a cell (Cotransport). Since Na + has a charge, and the glucose is neutral, the luminal membrane depolarizes (electrical transport). The contents of the digestive tube acquire a negative charge that contributes to reabsorption Cl - through dense intercellular contacts. Glucose leaves the cell through the baselateral membrane by the mechanism of lightweight diffusion (glucose carrier GLUT2). As a result, one spent mole ATP is rebucing 3 praying NaCl and 3 praying glucose. The mechanisms of reabsorption of neutral amino acids and a number of organic substances are similar to those described for glucose.B.- NaCl reabsorption due to the parallel activity of two carriers of the luminal membrane (a cushion, gallbladder). If a carrier exercising Na + / H + (antiport) is embedded in the cell furnace nearby, and the carrier that provides the exchange Cl - / HCO 3 - (antiport), then as a result of their operation, Na + and Cl ions will accumulate in the cell. In contrast to the NaCl secretion, when both carriers are located on the baselateral membrane, in this case both carriers are localized in the luminal membrane (NaCl reabsorption). The chemical gradient Na + is the driving force of the secretion of H +. H + ions go into the lumen of the digestive tube, and in the cell, it remains ions, which react with CO 2 (the reaction catalyst is carboangeerase). Anions HCO 3 is accumulated in the cell, the chemical gradient of which provides the driving force of the carrier transporting Cl - into the cell. CL - leaves the cell through basolateral cl ---channels. (In the lumen of the digestive tube H + and HCO 3 - react with each other with the formation of H 2 O and CO 2). In this case, it is reabsorbed 3 mole NaCl per 1 mol ATP

Sodium reabsorption in the Tolstoy Intestine

Mechanisms with which absorption in the thick intestine occurs, is somewhat different from the mechanisms that occur in the small intestine. Here you can also consider the two mechanisms that prevail in this department, which is illuminated in Fig. 10-23 as a mechanism 1 (Fig. 10-24 a) and mechanism 2 (Fig. 10-24 b).

Mechanism 1.(Fig. 10-24 a) prevails in the proximal department tolstoy intestine.Its essence lies in the fact that Na + gets into a cage through luminal Na + -Kanals.

Mechanism 2.(Fig. 10-24 b) is represented in the thick intestine due to K + / N + -ATPhase, located in the luminal membrane, the ions to + are rebupported.

Fig. 10-24. Reabsorption (absorption) Na + in the Tolstaya intestine.

AND- reabsorption Na + through luminal Na +.-Anals (primarily in the proximal division of the large intestine). On a cage-directed ion gradient Na +. can reabsorb, participating in the mechanisms of secondary active transport using carriers (cotransport or antiport), and enter the cell passively throughNa +.- channels (enac \u003d epithelial Na +. Channel) localized in luminal cell membrane. Just like in Fig. 10-23 A, this mechanism of Na + intake into the cell is electrical, therefore, in this case, the contents of the food tube lumen is negatively charged, which contributes to the reabsorption CL - through the intercellular tight contacts. The energy balance is, as in fig. 10-23 A, 3 praying NaCl on 1 mol ATP.B.- the work of H + / K + -ATFase contributes to the secretion of ions H + and reabsorptionk + ions on the mechanism of primary active transport (stomach, fat intestine). Due to this "pump" of the membrane of the stomach of the stomach, requiring the energy of ATP, H + 16 is accumulated in the lumen of the digestive tube in very high concentrations (this process is inhibited by omeprazole). H + / K + -ATFases in the thick intestine contributes to the reabsorption of KHCO 3 (brazed by ibain). On each secreted ion H + in the cell, ion Oh remains, which reacts with CO 2 (the reaction catalyst is carboangeerase) with the formation of HCO 3 -. HCO 3 - comes out of the shepherd cell through the baselateral membrane using the carrier providing the CL - / HCO 3 - (antiport; not shown here), the yield of HCO 3 - from the cell epithelial cell is carried out via HCO ^ -chanal. 1 mol reabsorbable KHCO 3 is spent 1 mol ATP, i.e. This is a rather "road" process. In this caseNa +./ K + -ATFAZ does not play a significant role in this mechanism, so it is impossible to identify the stoichiometric dependence between the amount of ATP spent and the amounts of substances

Exocrine pancreas function

Pancreaspossessed exocrine apparatus(along with endocrine part)which consists of cluster-shaped end plots - acinus(Palek). They are located at the ends of the branched duct system, the epithelium of which looks relatively monotype (Fig. 10-25). Compared to other exocrine glands in the pancreas, the complete absence of myoepithelial cells is especially noticeable. The latter in other glands support end areas during secretion when the pressure in the output duct increases. The absence of myoepithelial cells in the pancreas means that acinar cells during secretion are easily burst, so certain enzymes intended for exports into the intestine fall into the interface of the pancreas.

Ecocrine pancreatic departments

the digestive enzymes are isolated from the cells, which are dissolved in liquid with neutral pH and enriched with Ions Cl -, and from

the cells of the protruders are alkaline liquid-free from proteins. The digestive enzymes include amylases, lipases and proteases. Bicarbonate in the secret of the output cells is necessary for neutralizing hydrochloric acid, which comes with a chimus from the stomach in the duodenum. Acetylcholine from the endings of the wandering nerve activates the secretion in cells in cells, while the secretion of cells in the withdrawal ducts is stimulated primarily by secretin, synthesized in the S-cells of the mucous membrane of the small intestine. Due to the modulator influence on the cholinergic stimulation of cholecystokinin (SSC) affects the acinar cells, in the result of which their secretory activity is enhanced. Cholecystokinin also has a stimulating effect on the level of secretion of the cell of the pancreatic duct epithelium.

If the outflow of the secret is difficult, as in cystic fibrosis); If the pancreas juice is especially tight; Or when the output duct is narrowed as a result of inflammation or deposits, this can lead to inflammation of the pancreas (pancreatitis).

Fig. 10-25. The structure of the exocrine part of the pancreas.

At the bottom of the figure schematically, the existence that has already existed to date is the idea of \u200b\u200bthe branched system of the ducts, at the ends of which are the accins (end sites). An enlarged image shows that in reality the acinus is a network of interconnected secretory tubules. The introduced duct is connected through the subtle intra-roller duct with such secretory tubules

Mechanism of secretion of bicarbonate cells of the pancreas

Pancreas highlights about 2 liters of fluid per day. During digestion, the level of secretion increases many times as compared with the state of rest. At rest, an empty stomach, the level of secretion is 0.2-0.3 ml / min. After taking food, the level of secretion grows up to 4-4.5 ml / min. Such an increase in the speed of secretion in humans is the achievement of above all epithelial cells of output. While the acinuses release a neutral chloride juice with digestive enzymes dissolved in it, the epithelium of the output duct delivers alkaline fluid with a high bicarbonate concentration (Fig. 10-26), which is more than 100 mmol. As a result of the mixing of this secret with the National Assembly, the Himus pH containing ns1 rises to values \u200b\u200bin which digestive enzymes are assessed as much as possible.

The higher the speed of secretion of the pancreas, the higher concentration of bicarbonatein

pancreas juice. Wherein concentration of chloridebehaves like a mirror reflection of the bicarbonate concentration, therefore the sum of the concentrations of both anions at all levels of secretion remains the same; It is equal to the sum of ions K + and Na +, the concentrations of which are changed as slightly as the isotonicity of the pancreas juice. Such ratios of the concentrations of substances in the pancreas juice can be explained by the fact that two isotonic fluids are distinguished in the pancreas: one rich NaCl (acins), and the other rich nanox 3 (outputting ducts) (Fig. 10-26). In a state of rest and acinuses, and pancreatic ducts allocate a minor amount of secrecy. However, the secretion of acinuses prevails alone, as a result of which the final secret is rich in C1. When stimulating the gland secretthe level of secretion of the epithelium of the duct increases. In this connection, the chloride concentration is simultaneously reduced, since the amount of anions cannot exceed (unchanged) the amount of cations.

Fig. 10-26. The NaHCO 3 secretion mechanism in the pancreatic duct cells is similar to NAns0 3 sections in the intestine, since it also depends on the Na + / K + -at phase and the carrier protein localized on the basolateral membrane, which exercises the exchange of Na + / H + ions (antiport) through Basoolateral membrane. However, in this case, HCO 3 enters the rate of the gland not through the ion channel, but by means of a carrier protein that provides an anonal exchange. To maintain its operation, the connected parallel cl - -canal must ensure the recycling of the CL ions. This CL - -Kanal (CFTR \u003d CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR) defecten in patients with fibrosis (\u003d \u003dCysstic Fibrosis), what makes the secretion of the pancreas more damping and poor HCO 3 -. The liquid in the infection of the gland is charged negatively relative to the interstitial as a result of the exit from the CL cell - into the lumen of the duct (and the penetration of K + into the cell through the baseoolateral membrane), which contributes to the passive diffusion of Na + in the base of the gland for intercellular tight contacts. The high level of secretion of HCO 3 is possible, apparently, because HCO 3 is secondaryly actively transported into a cell using a carrier protein that performs the associated transport Na + -HCO 3 - (Symport; NBC carrier protein, in the figure is not depicts; SITS carrier protein)

Composition and properties of pancreatic enzymes

Unlike the cells of the duct, the acinar cells allocate digestive enzymes(Table 10-1). In addition, the acinuses supply nonferred proteins,such as immunoglobulins and glycoproteins. Digestive enzymes (amylases, lipases, proteases, dnise) are needed for normal digestion of composite parts of food. There are data

that the set of enzymes varies depending on the composition of the accepted food. Pancreas to protect themselves from self-extinguishing with its own proteolytic enzymes, highlights them in the form of inactive precursors. So trypsin, for example, secreted in the form of a trypsinogen. As an additional protection, the pancreas juice contains a trypsin inhibitor, which prevents its activation inside the secretory cells.

Fig. 10-27. Properties of the most important digestive enzymes of the pancreas, isolated by acinar cells, and acinar neferredic proteins (Table 10-1)

Table 10-1. Pancreatic enzymes

* Many digestive pancreatic enzymes exist in two or more forms that differ from each other with relative molecular masses, optimal pH and isoelectric dots

** ENZYME COMMISTION CLASSIFICATION SYSTEM, INTERNATIONAL UNION OF BIOCHEMISTRY

Endocrine pancreas function

Isle apparatusis endocrine part of the pancreasand only 1-2% of the tissue is preferably an exocrine part. Of these, about 20% - α -Lesters,in which glucagon is formed, 60-70% are β -Lesters,which produce insulin and amylin, 10-15% - Δ -Lesters,which synthesize somatostatin, inhibiting insulin and glucagon secretion. Another type of cells - F-cellsit produces pancreatic polypeptide (other name - PP cells), which is possible is a cholecystokinin antagonist. Finally, there are also G-cells producing gastrin. The quick modulation of the release of hormones in the blood provides localization of these endocrine active cells in the Union with Islands of Langerhans (called

so in honor of the opener - German studentman), allowing to implement parakrin controland additional direct intracellular transport of substances of transmitters and substrates through numerous Gap Junctions(dense intercellular contacts). Insofar as V. Pancreatica.blows into a portal vein, the concentration of all pancreatic hormones in the liver, most important to metabolism by the organ, is 2-3 times higher than in the rest of the vascular system. When stimulated, this ratio increases 5-10 times.

In general, endocrine cells allocate two key for the regulation of hydrocarbon exchangehormone: insulinand glucagon.The secretion of these hormones mainly depends on blood glucose concentrationsand modulated somatostatin,the third most important hormone islets, together with gastrointestinal hormones and the autonomous nervous system.

Fig. 10-28. Island Langerhansa

Glucagon and insulin-hormones of the pancreas

Glucagonit is synthesized in α. Blots.Glucagon consists of a single chain of 29 amino acids and has a molecular weight of 3500 DA (Fig. 10-29 A, b). Its amino acid sequence is homologous to some gastrointestinal hormones, such as secretine, vasoactive intestinal peptide (VIP) and GIP. From an evolutionary point of view, this is a very old peptide that has retained not only its form, but also some important functions. Glucagon is synthesized through prephorormon in the α-cells of the islands of the pancreas. The human peptide glucagon in humans are also additionally formed in various intestinal cells. (Enteroglyukonor GLP 1). The post-translation splitting of the priscloth in various intestinal cells and the pancreas occurs in different ways, so that a number of peptides are formed, the functions of which are not yet clarified. Blood circulating glucagon is about 50% connected to plasma proteins; this so-called large glucagon plasma,biologically not active.

Insulinit is synthesized in β Blots.Insulin consists of two peptide chains, a chains of 21 and a chain of 30 amino acids; Its molecular weight is about 6000 Da. Both chains are interconnected by disulfide bridges (Fig. 10-29 c) and are formed from the predecessor, proinsulinas a result of the proteolytic cleavage of C-chain (binding peptide). The gene for the synthesis of insulin is localized in the 11th human chromosome (Fig. 10-29 g). With the help of appropriate mRNA in the endoplasmic reticulum (ER) synthesized preproynsulinwith molecular weight of 11,500 DA. As a result of separating the signal sequence and formation of disulfide bridges between the chains A, B and C appears, which in the microvi

kulach is transported to the Golgi apparatus. There is a cleavage of the C-chain from the epsulin and the formation of zinc-insulin-hexamers - the inventory form in the "mature" secretory granules. We clarify that insulin of different animals and humans differ not only in the amino acid composition, but also by α-helix, which causes the secondary structure of the hormone. A more complex is a tertiary structure, forming sections (centers) responsible for biological activity and antigenic properties of the hormone. The tertiary structure of monomeric insulin comprises a hydrophobic cine, which forms a semi-shaped process on its surfaces with hydrophilic properties, with the exception of two non-polar regions that ensure the aggregation properties of the insulin molecule. Internal structure of insulin molecule is important for interacting with its receptor and manifestations of biological action. When studying with X-ray structural analysis, it was established that one hexamecaric unit of crystalline zinc insulin consists of three dimers, rolled around the axis, on which two zinc atoms are located. Proinsulin as well as insulin forms dimers and zinc-containing hexameras.

During exocytosis, insulin (a- and in-chain) and C-peptide are allocated in equimolar quantities, and about 15% of insulin remains as a proinsulin. The Prosulin itself provides only a very limited biological effect, there are no significant information about the biological effect of C-peptide. Insulin has a very short period of half-life, about 5-8 minutes, from the C-peptide - 4 times longer. In the clinic, the plasma C-peptide measurement is used as the parameter of the functional state of β-cells, and even with insulin therapy makes it possible to estimate the residual secretory container of the endocrine pancreas.

Fig. 10-29. The structure of glucagon, proinsulin and insulin.

AND- glucagon is synthesized inα Blots and its structure is presented in the panel. B.- Insulin is synthesized inβ Blots. IN- in the pancreasβ -Lesters that produce insulin are equally distributed, whileα-cells producing glucagon are concentrated in the talle of the pancreas. As a result of the cleavage of C-peptide, insulin consisting of two chains appears in the specified areas:ANDand V. G.- Insulin synthesis scheme

Cellular insulin secretion mechanism

Pancreatic β cells increase the level of intracellular glucose due to its entry through the GLUT2 conveyor and metabolized glucose, as well as galactose and mannose, and each of this substance can cause insulin secretion by islands. Other hexoses (for example, z-o-methylglucose or 2-dexyglucose), which are transported in β-tickets, but cannot be metabolized there, and does not stimulate insulin secretion. Some amino acids (especially arginine and leucine) and small ketocislotes (α-keetoisocaproate) just like ketohexoses(fructose), may weakly stimulate the secretion of insulin. Amino acids and ketokislotes do not share any metabolic path with hexoses except oxidation through citric acid cycle.These data led to the assumption that ATF, synthesized as a result of the metabolism of these different substances can be involved in the secretion of insulin. Based on this, 6 stages of insulin secretion of β-cells were proposed, which are set forth in the dying signature to Fig. 10-30.

Consider the whole process in more detail. Insulin secretion mainly manages blood glucose concentration,this means that food intake stimulates secretion, and with a decrease in glucose concentration, for example, during starvation (post, diet), the emission is inhibited. Usually insulin is secreted with an interval of 15-20 minutes. Such pulsation secretion,apparently, it matters for insulin efficiency and provides an adequate function of insulin receptors. After stimulating the secretion of insulin intravenous administration of glucose is observed two-phase secretory response.In the first phase, the maximum insulin release occurs within minutes, which in a few minutes weakens again. After about 10 minutes, the second phase occurs with the continued enhanced insulin secretion. It is believed that both phases meet various

insulin stocking forms. It is also possible that various Parakrine and auto regulatory mechanisms of islet cells are responsible for such two-phase secretion.

Stimulation mechanisminsulin secretion with glucose or hormones is largely clarified (Fig. 10-30). Decisive is an increase in concentration ATFas a result of glucose oxidation, which, with an increase in the concentration of glucose in plasma, with the help of a transported transporter in an increased quantity enters β-cells. As a result of ATP- (or on ATP / ADF ratio), the dependent K + -Kanal is inhibited and the membrane depolarizes. As a consequence, potential-dependent C 2+ - channels, the extracellular CA 2+ rushes inside and activates the process of exocytosis. The pulsation release of insulin is a consequence of a typical sample of the discharge of β-cells "packs".

Insulin's cellular mechanismsvery diverse and not yet completely clarified. The insulin receptor is a tetradimer and consists of two extracellular α-subunits with specific binding places for insulin and two β-subunits that have transmembrane and intracellular parts. The receptor refers to the family tyrosine kinase receptorsand it is very similar in structure with somatomatin-C- (IGF-1-) receptor. The β-subunit of the insulin receptor on the inside of the cell contain a large number of tyrosine kinase domains, which in the first stage are activated using autophosphorylation.These reactions are essential to activate the following kinases (for example, phosphatidylositol 3-kinases), which then induce various phosphorylation processes, with the help of which in effector cells, the majority of enzymes involved in the metabolism are activated. Besides, internalizationinsulin, along with its receptor in the cell, it is also possible to express specific proteins.

Fig. 10-30. Insulin secretion mechanismβ -Lesters.

Increasing the level of extracellular glucose is a trigger for secretionInsulin β-cells, which occurs in the form of seven stages. (1) Glucose enters the cell through the GLUT2 conveyor, the work of which is mediated by the lightweight glucose diffusion into the cell. (2) An increase in glucose input stimulates the metabolism of glucose in the cell and leads to an increase in [ATP] i or [ATP] I / [ADP] i. (3) Increase [ATP] I or [ATP] I / [ADP] I inhibits ATP-sensitive to + -Kanal. (4) Inhibition of ATP-sensitive to + -Kanalov causes depolarization, i.e. V M acquires more positive values. (5) Depolarization activates potential-controlled Ca 2+ - cell membranes of cells. (6) Activation of these potential-controlled Ca 2+ -Channels increases the input of C C 2+ and, thus, increases I, which also causes Ca 2+-induced Ca 2+ -Relliza from the endoplasmic reticulum (er). (7) The accumulation of I leads to exocytosis and exit in the blood of insulin contained in secretory granules

Ultrastructure of the liver

The ultrastructure of the liver and biliary tract is shown in Fig. 10-31. Bile is highlighted by the cells of the liver into the biliary tubules. The biliary tubules, merging with each other on the periphery of the hepatic slices, form larger biliary moves - perilobular bile ducts lined with epithelium and hepatocytes. Perilobular bile grooves fall into interdolk bile ducts lined with cubic epithelium. Anastomosing between

in size and increasing in size, they form large septal ducts, surrounded by a fibrous cloth of portal paths and merging into the equity left and right hepatic ducts. On the lower surface of the liver in the region of the transverse groove, the left and right hepatic ducts are connected and form a common liver duct. The latter, merging with the bubble duct, flows into the overall biliary duct, opening into the lumen of the duodenum in the region of a large duodenal duodenum region, or a nipple factor.

Fig. 10-31. Liver ultrastructure.

The liver consists ofpole (diameter 1-1.5 mm), which on the periphery are supplied with portal vein branches(V.Portae) and liver artery(A.Hepatica). The blood of them proceeds through the sinusoids, which supply hepatocyte blood, and then falls into the central vein. Between hepatocytes, there are tube, closed on the side with tight contacts and do not have the own wall of the gap, bile capillaries or tubules, Canaliculi Biliferi. It is allocated bile (see Fig. 10-32), which leaves the liver through the bile stroke system. The hepatocytes of the epithelium corresponds to the terminal departments of the usual exocrine glands (for example, salivary glands), the biliary tubules are the lumen of the terminal department, the bile ducts - the withdrawing glands, and the sinusoids - blood capillaries. It is unusual that sinusoids are obtained by a mixture of arterial (rich O 2) and the venous blood portal veins (poor O 2, but rich in nutritious and other substances coming from the intestine). Krafe cells are macrophages

Composition and secretion of bile

Bileit is an aqueous solution of various compounds with the properties of a colloidal solution. The main components of bile are bile acids (chill and in a small amount of deoxychole), phospholipids, biliary pigments, cholesterol. The composition of the bile also includes fatty acids, protein, bicarbonates, sodium, potassium, calcium, chlorine, magnesium, iodine, a slight amount of manganese, as well as vitamins, hormones, urea, uric acid, a number of enzymes, etc. In the bustling bubble Concentration of many components 5-10 times higher than in the hepatic. However, the concentration of a number of components, such as sodium, chlorine, bicarbonates, due to their absorption in the bustling bubble is significantly lower. Albumin, present in the hepatic bile, is not at all detected in the bubble.

Bile is formed in hepatocytes. In hepatocyte, two poles are distinguished: vascular, carrying out with the help of microvascular seizure of substances from the outside and the introduction of them into the cell, and biliary, where substances from the cell occurs. The microvilles of the biliary pole of hepatocyte form the origins of the biliary tubules (capillaries), the walls of which are formed by membranes

two or more adjacent hepatocytes. The formation of bile begins with the secretion of water hepatocytes, bilirubin, bile acids, cholesterol, phospholipids, electrolytes and other components. The secretioning apparatus of hepatocyte is represented by lysosomes, a plate complex, microwaves and bustling tubules. Secrecy is carried out in the microvascular zone. Bilirubin, bile acids, cholesterol and phospholipids, mainly lecithin, are distinguished in the form of a specific macromolecular complex - bile micelles. The ratio of these four main components, quite constant normally, ensures the solubility of the complex. In addition, the small solubility of cholesterol increases significantly in the presence of bile acid salts and lecithin.

The physiological role of bile is mainly connected with the process of digestion. The most important importance for digestion is bile acids that stimulate the secretion of the pancreas and have an emulsifying effect on fats, which is necessary for their digestion of pancreatic lipase. Bile neutralizes the acidic content of the stomach entering the duodenum. Bile proteins are able to bind pepsin. Alien substances are excreted with bile.

Fig. 10-32. Secretion of bile.

Hepatocytes highlight electrolytes and water into the biliary tubules. Additionally, hepatocytes are isolated primary bile salts, which they are synthesized from cholesterol, as well as secondary bile salts and primary bile salts, which they are captured from sinusoids (intestinal hepatic recycling). The secretion of bile acids is accompanied by additional secretion of water. Bilirubin, steroid hormones, alien substances and other substances are associated with glutathione or glucuronic acid, to increase their solubility in water, and in such a conjugated form are highlighted in bile

Synthesis of bile salts in the liver

The bile liver contains bile salts, cholesterol, phospholipids (primitive phosphatidylcholine \u003d lecithin), steroids, as well as exchange products, such as bilirubin, and many alien substances. Bile isotonic blood plasma, and its electrolyte composition is similar to the electrolyte composition of blood plasma. The pH value is neutral or slightly alkaline.

Bile saltsare cholesterol metabolites. The bile salts are captured by hepatocytes from the blood of portal veins or are synthesized intracellularly, after conjugation with glycine or taurine through the apical membrane into the biliary tubules. The biliary salts form micelles: in bile - with cholesterol and lecithin, and in the lumen of the intestine - primarily with poorly soluble lipolysis products for which the necessary prerequisite for reabsorption is the formation of micelles. With the reabsorption of lipids, the bile salts are released again, reabsorbed in the end departments of the ileum and so again fall into the liver: the gastrointestinal circuit. In the epithelium of the large intestine, bile salts increase the permeability of the epithelium for water. The secretion of both bile salts and other substances is accompanied by water movements along osmotic gradients. The secretion of water due to the secretion of bile salts and other substances is in each case 40% of the amount of primary bile. The remaining 20%

water falls on liquids allocated by the cells of the epithelium of the gall duct.

The most common bile salts- Soli. chill, hyperode (h) oxychole, de (h) oxyhole and lithocholeumbile acids. They are captured by the liver cells from the blood of a sinusoid using an NTCP carrier (Cotransport with Na +) and an OATP carrier (independent of Na + transfer; OATP \u003d O.rganic. A.nion. -T.ransporting. P.olypeptide) and in hepatocytes form a conjugate with amino acids, glycin or Taurin(Fig. 10-33). Conjugationpolarizes the molecule from the amino acid, which facilitates its solubility in water, while the steroid skeleton is lipophile, which facilitates interaction with other lipids. Thus, conjugated bile salts can perform function detergents(substances providing solubility) for usually poorly soluble lipids: When the concentration of bile salts in bile or in the lumen of the small intestine exceeds a certain (so-called critical micellar) value, they spontaneously form the smallest aggregates with lipids, micelles.

The evolution of various bile acids is associated with the need to hold lipids in the solution in a wide range of pH values: at pH \u003d 7 - in bile, at pH \u003d 1-2 - in the chimney coming from the stomach and at pH \u003d 4-5 - after the chimus is mixed with pancreatic juice. This is possible due to different RKA " -Notions of individual bile acids (Fig. 10-33).

Fig. 10-33. Synthesis of bile salts in the liver.

Hepatocytes, using cholesterol as the initial substance, form biliary salts, primarily dryheloxy cholate and cholat. Each of these (primary) bile salts can be conjugated with an amino acid, first of all with a taurine or glycine, which reduces the PKA "salt from 5 to 1.5 or 3.7, respectively. In addition, the part of the molecule shown in the figure on the right becomes Hydrophilic (middle part of the figure). Of the six different conjugated bile salts, both kolata conjugate with their complete formulas are shown on the right. The conjugated bile salts are partially deconcted by bacteria in the lower divide department and then dehydroxylized in the C-atom, thus, from primary hegeneroxichet bile salts and The cholata is formed by secondary bile salts of Litocholate (not shown in the figure) and deoxycholate, respectively. The latter fall as a result of intestinal and liver recirculation again into the liver and re-form conjugates to take part in the reabsorption of fats after secretion

Intestinal and liver circuit of bile salts

For digestion and reabsorption 100 g fat, about 20 g bile salts.Nevertheless, the total amount of bile salts in the body rarely exceeds 5 g, and only 0.5 g is synthesized daily (cholate and minodoxycholate \u003d \u003d primary bile salts).Successful fat absorption using a small amount of bile salts is possible due to the fact that in the ileum 98% allocated with bile of bile salts is reabsorbed by the mechanism of secondary active transport in conjunction with Na + (Cotransport), enters the blood of the portal vein and returns to the liver: intestinal and hepatic recycling(Fig. 10-34). On average, this cycle is repeated for one bile salt molecule up to 18 times before it is lost with the feet. In this case, conjugated bile salts decongy

in the lower part of the duodenum with bacteria and decarboxylaim, in the case of primary bile salts (education secondary bile salts;see fig. 10-33). In patients whose surgically removed the iliac or which suffer from chronic intestinal inflammation (Morbus Crohn),most of the bile salts are lost with the feces, so digestion and suction of fats are disturbed. Steatery(fat chair) and malabsorptionare the consequences of such violations.

It is interesting that a small percentage of bile salts, which falls into a thick intestine, plays an important physiological role: bile salts interact with lipids of luminal cell membrane and increase its permeability to water. If the concentration of bile salts in the thick intestine decreases, the reabsorption of water in the thick intestine decreases and, as a result, develops diarrhea.

Fig. 10-34. Intestinal and hepatic recycling of bile salts.

How many times the day the pool of bile salts circulates between the intestines and the liver, depends on the content of fat in food. When digesting normal food, the pool of bile salts circulates between the liver and the intestines 2 times a day, with rich foods, the circulation occurs 5 times or more often. Therefore, the numbers in the figure give only an approximate representation.

Bile pigments

Bilirubinit is formed mainly when hemoglobin cleavage. After the destruction of the macrophages of the reticuloendothelial system from hemoglobin, the rings of the hem, and after the destruction of the hemoglobin ring, turns first into biliverdin and then in bilirubin. Bilirubin, by virtue of its hydrophobicity, is transferred by plasma blood in the associated albumin. From the plasma of blood bilirubin is captured by the cells of the liver and binds to intracellular proteins. Then bilirubin forms conjugates with the participation of glucuronyltransferase enzyme, turning into water-soluble mono- and Diglucronides.Mono- and Diglucuronides with the help of a carrier (MRP2 \u003d CO), the work of which requires the cost of energy ATP, stand out into the bulls.

If the content of a bad soluble, non-conjugated bilirubin increases in bile (usually 1-2% micellar "solution"), regardless of dependence, this is due to the overload of glucuronyltransferase (hemolysis, see below), or as a result of damage to the liver or bacterial deconjugation in bile, then The so-called are formed pigmed stones(calcium billarinate, etc.).

Fine bilirubin concentration in blood plasmaless than 0.2 mmol. If it increases to the value greater than 0.3-0.5 mmol, then the blood plasma looks like yellow and connective tissue (first the scler, and then the skin) are painted in yellow, i.e. Such an increase in bilirubin concentration leads to joy (ICTERUS).

The high concentration of bilirubin in the blood can have several reasons: (1) the mass death of the erythrocytes for any reason, even with normal liver function increases in

blood plasma Concentration of non-conjugated ("indirect") bilirubin: hemolytic jaundice.(2) The glucuronyltransferase enzyme defect also leads to an increase in the number of non-conjugated bilirubin in the blood plasma: hepatocellular (hepatic) jaundice.(3) Postgepathite jaundiceit occurs when the biliary tract occurs. It can happen like in the liver (Host),and beyond its limits (as a result of the occurrence of a tumor or stone in Ductus Choleodochus):mechanical jaundice.Bile accumulates above the location of the blockage; It is squeezed together with conjugated bilirubin from the biliary tubules through the desplaomomomas in the extracellular space, which is associated with the sine of the liver and, thus, with linen veins.

Bilirubinand its metabolites are reabsorbed in the intestines (about 15% of the amount allocated), but only after they are cleaved (anaerobic intestinal bacteria) glucuronic acid (Fig. 10-35). Free bilirubin is converted by bacteria in urobilinegen and sterkobilinogen (both colorless). They are oxidized to (painted, yellow-orange) finite products urobiland sterkobilo,respectively. A small part of these substances falls into the blood of the circulatory system (primarily urobilinogen) and after glomerular filtration in the kidney turns out to be in the urine, giving it a characteristic yellowish color. At the same time, the end products remaining in feces, urobilin and sterkobilin, paint it in brown. With a rapid passage by the intestines, the invisible bilirubin stains the powerful masses in the yellowish color. When in the cartoons, like bilirubin, neither the products of its decay, are not detected, or the products of its decay, the consequence of the gray color of the feces.

Fig. 10-35. Bilirubin removal.

A day is excreted to 230 mg of bilirubin, which is formed as a result of hemoglobin cleavage. In the blood plasma Bilirubin is associated with albumin. In liver cells, with the participation of glucuroneransferase, bilirubes forms a conjugate with glucuronic acid. Such conjugated, significantly better soluble in water bilirubin is highlighted in bile and falls into a thick intestine. There, the bacteria split the conjugate and convert free bilirubin in urobilinogen and sterkobilinogen, from which urobilin and sterkobilin, which give the chair brown, are formed as a result of oxidation. About 85% of bilirubin and its metabolites are displayed with a chair, about 15% reabsorbed again (intestinal and hepatic circulation), 2% falls through the circulatory system in the kidneys and is removed from the urine

Small intestine

The delicious intestine provides the final digestion of food, absorbing all nutrients, as well as mechanical food advancement towards the thick bowel and some evacuator function. In the small intestine distinguish several departments. The plan for the structure of these departments is the same, but there are some differences. The relief of the mucous membrane forms circular folds, intestinal patches and intestinal crypts. Folds are formed by the mucous membrane and the submucosal base. Vilki is a finger-shaped rose of own plates covered on top of the epithelium. Crypts are the recesses of the epithelium into its own plate of the mucous membrane. Pieces, lining the slim intestine - single-layer prismatic. In this epithelium distinguish:

• Stroll enterocytes
• Box and shaped cells
• M cells
• Patenet cells (with acidophobic grain)
• Endocrine cells
• Undifferentiated cells

1. EC cells produce serotonin
2. ECL cells produce histamine
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