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Structural changes of duodenal mucosa enterocytes of rats in burn skin injury under experimental streptozotocin-induced diabetes mellitus

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.