Circulatory disorders and mucous barrier

It is known that the mucosa of the stomach is not the end of the arteries, and they break down into network arterioles and capillaries, anastomosed with each other on different levels. In the submucosal layer are arteriovenous shunts and distribution of blood flow in the mucous determined by two parameters of resistance, one - in arterioles and the other in arteriovenous shunts. A similar structure is the system of blood circulation in the duodenum. It is possible that when ulcers hypertonicity stray nerves and Hyper-reactivity of the cortex of the adrenal glands can cause transient disturbances in shunt blood circulatory system, manifested either stagnant plethora (closing of shunts)or local ischemia (opening shunts). Both types of disorders cause hypoxia mucosa, changing its structure and increase their vulnerability. The lack of available clinic method of studying circulation in the lining of the stomach does not allow to confirm logical assumptions about the value of these violations in formation. Introduction into clinical practice of selective angiography of the stomach (M. I. Kuzin, etc., 1969), probably, will fill the existing gap.
Gastric mucus arises from two sources: mukodni cells necks major glands of the stomach that produces mucoproteins and superficial epithelial lining of the stomach that produce so-called visible mucus.
Hollander (1962) thought that the mucus barrier consists of two components: a layer of viscous mucus secretion and layer sliseobrazutee epithelium, located under the cells of the gastric glands. Both layers function as one unit and ensure a "blurring" the mucosal surface. P. D. Rabinovich (1967) allocates the third component of gastric barrier - mucous substances contained in the tissues located deeper mucosa.
In gastric secret in healthy persons detected neutral and acid mucopolysaccharides, Glyco - and mukoproteidov present mainly in the composition of visible mucus. The last under the mucolytic action of the enzyme - "stomach of musalitina" - collapses and forms a faction mucoprotein". The mukoproteidov very rich Fuksas, in connection with what they called the "fukomuzinov" (C. S. Yurkova and others, 1969). According to P. D. Rabinovich, in the period of exacerbation of ulcer content of fucose in the mucous membrane was normal, but it decreased sharply in the gastric mucus, which can be explained by the violation of allocation of focalizing in the gastric lumen. In the phase of remission, the concentration of fucose in the gastric mucus increased. C. S. Yurkova, and others were similar results only in patients with peptic ulcer with normal structure of the gastric mucosa, and in the presence of associated gastritis content fucose was determined to be high. The active phase of chronic gastritis in the gastric mucus and the lining of the stomach increases the total number of mucopolysaccharides, which are dominated by neutral mucopolysaccharides. At the beginning of atrophic gastritis increases the acid sulfatirovannah mucopolysaccharides. Excessive their products violates the autoregulation of regenerative processes, trophic changes of the mucous membrane of the stomach (E. F. Kanaev, 1965). Describes the qualitative and quantitative changes in the mucus may play a role in the formation of ulcers. It is known that the chronic gastritis almost always combined with gastric ulcer, it is considered above violations of sliseobrazutee.
Changes in structure mucopolysaccharides gastric mucus with a predominance of acid mucopolysaccharides, containing fucose, lead to an increase in the viscosity of mucus. Increase of viscosity can serve as a protective factor that protects the stomach lining from samoupravlanja in conditions hypersecretion. On the other hand, viscous mucus may be worse than usual, to protect mucous membrane duodenal ulcer from ulcerogenic impacts. In addition, a layer of viscous mucus can also block the receptor pH in the antrum of the stomach and thereby violated the physiological mechanism of self-regulation of allocation of hydrochloric acid, which is manifested by its inhibition of lowering the pH in the lumen of the stomach. In the absence of antral inhibition of secretion of hydrochloric acid mucosa of the duodenum is subjected to prolonged exposure to diluted acid gastric juice (Curt and Pringle, 1969).