Роль стресу в патогенезі пептичної виразки гастродуоденальної зони

Abstract

В статті наведені сучасні наукові дані щодо ролі стресових чинників в патогенезі пептичної виразки шлунка та дванадцятипалої кишки. Висвітлені механізми ураження слизового бар’єра гастродуоденальної зони за рахунок порушення вегетативної регуляції, деполімерації мукопротеїнів слизового бар’єра шлунка, активації оксидативного стресу на тлі ураження мікроциркуляторного русла. Наведені дані доводять суттєву роль стресу як кофактору ульцерогенезу на тлі інфікування Helicobacter pylori. ; В статье приведены современные научные данные о роли стрессовых факторов в патогенезе язвенной болезни желудка и двенадцатиперстной кишки. Освещены механизмы повреждения слизистого барьера гастродуоденальной зоны за счет нарушения вегетативной регуляции, деполимерации мукопротеинов слизистого барьера желудка, активации оксидативного стресса на фоне поражения микроциркуляторного русла. Приведенные данные показывают существенную роль стресса как кофактора ульцерогенеза на фоне инфицирования Helicobacter pylori. ; Peptic ulcer (PU) of the stomach and duodenum refers to the most urgent problems of modern gas-troenterology. The main etiological factors of ulcer formation in the gastroduodenal zone (GDZ) are hereditary pre-disposition to PV, infection of Helicobacter pylori (HP), types of nervous and endocrine regulation, immune status of the cytokine profile, neuroimunuodocrine disorders. The direct influence of stress factors on the course of peptic ulcer is confirmed by the significant increase of this pathology during military conflicts, economic depression and natural disasters. The article presents modern scientific data on the role of stress factors in the pathogenesis of PU of the stomach and duodenum. The mechanisms of damage to the mucous barrier of the GDZ due to the violation of autonomic regulation, depolymerization of mucoproteins of the mucous barrier of the stomach, activation of oxidative stress against the background of the lesion of the microcirculatory bed are discussed. The data presented show the es¬sential role of stress as a cofactor of ulcerogenesis against the background of infection with HP. In the implementation of the stress response, the leading role belongs to the hypothalamo-reticular structures of the brain that interact closely with the hippocampus and form a single hypothalamic-pituitary-adrenocortical system that directly affects neuroendocrine regulation of the synthesis of biologically active substances, hydrochloric acid, microcirculation processes and immune defense of the mucous GDZ, motor function of the stomach. Important in the processes of cytoprotection under the conditions of chronic stress is the balance of protective factors, among which one of the most important recognized products of high-grade mucins (glycoproteins), the composition and properties of which determines the condition of the mucosal barrier on the surface of the epithelial cells. Under the influence of stress factors, the destruction of the connective tissue structures of GDZ occurs, as evidenced by the likely increase in the concentration of N-acetylneuramic acid (NANA) in serum. In the process of development of an experimental ulcer of the stomach, the intensity of lipoperoxidation is sharply increased, which is a universal mechanism of damage to cell membranes. The activation of peroxidation processes was confirmed by the probable increase in the content of TBK-active products against the background of a decrease in antioxidant activity due to redistribution of antioxidants in the body, violation of their absorption, increased catabolism at the centre of the lesion. The previous adaptation to the stressful effects of an experimental ulcer of the stomach promotes the activation of antioxidant systems of the body against the suppression of lipo¬peroxidation, which prevents the damage to the cells of the SBP, the development of the inflammatory process, vasoconstriction, and, accordingly, cell apoptosis. The morphological substrate for experimental PU is a significant damage to GDZ, characterized by destruction and expansion of the diameter of the fundus glands of the stomach, dilatation of the vessels of the microcirculatory bed and thickening of the vessels of the submucosal vessels and other membranes. A significant number of parietal cells found in a state of unsteadily expressed necrobiosis have been detected, and the expansion of the interstitite space and the presence of connective tissue in it. The revealed structural changes indicate the suppression of re¬gional microcirculation, which proves the essential role of hypoxia in ulcerogenesis. Thus, stress factors play an important role in the pathogenesis of defeat of the mucosal barrier of GDZ, affecting the main factors of gastric homeostasis.