The work is devoted to the study of structural changes of enterocytes in the mucous membrane of the duodenum in a burn injury of the skin of a rat under conditions of experimental streptozotocin induced diabetes. The study was carried out on laboratory white adult rats-males weighing 180-210 g. The control group consisted of 21 animals without somatic pathology, the first experimental group consisted of 21 rats with skin burn injury, the second experimental group cleared 21 rats with skin burn and experimental streptozotocin induced diabetes. A model of experimental diabetes mellitus was reproduced by administering streptozotocin intraperitoneally once in dose of 50 mg/kg to rats. In an experimental simulation of a skin burn, two copper plates in the form of an ellipse were kept in water at 100oC for 10 minutes and, under ether anesthesia conditions, were applied simultaneously symmetrically on both exposed parts of the body of rats with an exposure for 10 seconds. Burn skin damage in rats was II-AB degrees – dermal surface burn (according to the old classification III-A degree) with a total area of 21-23% of the body surface with the development of burn shock. For morphological studies, the duodenum was taken, fragments of which were processed using conventional light and electron microscopy. The main criteria for assessing damage the enterocytes of the duodenal mucosa were the results studies of histological and ultrastructural data over 7, 14 and 21 days after a skin burn. The results of the studies showed that the damage of the enterocytes of the duodenal mucosa is based on deep destructive changes, which after 21 days (at the stage of septic toxemia), as a rule, are not reversible and develop against the background of significant intoxication of the organism. In the mucous membrane of the duodenum with burn injury of the skin associated with diabetes mellitus, there is a deterioration of the manifestations of the adaptive response and prolongation of destructive processes, accompanied by a violation of intercellular interactions in cytoarchitectically modified and deformed villi and crypts.

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The aim of the study was to study the structural changes of the intestinal epithelial barrier in the duodenum in burn injury of skin in rat under experimental streptozotocin-induced diabetes mellitus. The study was carried out on laboratory white adult rats-males weighing 180-210 g. The control group consisted of 21 animals without somatic pathology, the first experimental group was 21 rats with burn skin injury, the second experimental group was 21 rats with burn skin and experimental streptozotocin-induced diabetes mellitus. The experimental diabetes model was reproduced by administering streptozotocin to the rats intraperitoneally at a single dose of 50 mg/kg. Thermal burn skin damage in rats corresponded to II – A-B degrees of dermal surface burn (according to the old classification III – A degree) with a total area of 21-23 % of the body surface with the development of burn shock. Duodenum was selected for morphological studies, fragments of which were processed by conventional methods of light and electron microscopy. The main criteria for assessing damage to the duodenal mucosa enterocytes were the results of a study comparing histological and ultrastructural data in dynamics at 7, 14, and 21 days after skin burns. The results of the studies showed that the base of damage to the intestinal epithelial barrier of the duodenum are deep destructive changes, which after 21 days (in the stage of septicotoxemia), as a rule, are not reverse and develop on the background of significant intoxication of the body. There was a decrease in the number of tight junctions in the intestinal epithelial barrier of the duodenum of rats of the first and second experimental groups and a loss of ordering (acquisition of some chaotic nature) of their localization as the time after burn injury increased. For the most part, the intestinal epithelial barrier loses the integrity of the cellular component with partial preservation of the basement membrane (the first occurs both due to necrosis of the enterocytes with a brush border and due to complete destruction of goblet cells). In all cases, defects exist in the intestinal epithelial barrier, which are potential pathways for paracellular translocation of the pathogenic contents of the duodenum. It is not inconceivable that part of this intestinal pathogenic content can be translocated also by partially damaged cells. Evidence of the latter is the presence of microbial bodies in the cytoplasm of cells with partially destroyed plasmalemma (but preserved organelles and nucleus). An adaptive mechanism for ensuring the repair of damaged enterocytes is selective autophagy, which acts as a factor in the recycling of destroyed organelles and the cytoplasmic matrix, aimed primarily at maintaining cell viability.