ROLE OF ENDOTHELIAL DYSFUNCTION IN PATHOGENESIS OF ENTERAL INSUFFICIENCY

The study aims to establish the features of the severity of endothelial dysfunction in case of enteral insufficiency in various models of acute surgical pathology by assessing the concentration of adhesion molecules PECAM-1 (CD31) in the blood plasma of experimental animals. Material and methods. The experiment was carried out on 25 male Chinchilla rabbits with an average weight of 2,700 ± 100 g, which were divided into 3 groups: five intact animals in group I, group II with ten rabbits in which peritonitis was modeled, group III included ten animals with acute intestinal obstruction. Mortality due to the progression of the pathological process was 8 % (two rabbits) on the 3rd day of the experiment. Throughout the experimental study, the intra-abdominal pressure was measured by a direct method. To assess the severity of intra-abdominal hypertension in animals, the indices corresponding to the
norms of intra-abdominal pressure for humans were recalculated. The experiment investigated the concentration of adhesion molecules PECAM-1 (CD31) in all groups and evaluated the pathomorphological picture of the state of the small intestine and microvasculature in acute intestinal obstruction and peritonitis. Results. In animals in group II, the concentration of CD31 was statistically significantly higher (p <0.05) compared to those in group III, where the process of acute intestinal obstruction was simulated throughout the entire experiment, which indicates more severe damage to the vascular endothelium and impaired tone of the microvasculature. When analyzing the data of measurements of intra-abdominal pressure, no statistically significant differences were found between the two groups of animals. The pathological picture of the wall of the small intestine and the microvasculature depends on the stage of inflammation and the level of intra-abdominal pressure during the progression of enteral insufficiency.

peritonitis, acute intestinal obstruction, enteral insufficiency, endothelial dysfunction, adhesion molecules, microcirculation, mechanosensory complex PECAM-Flk-1.

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