PATHOGENETIC FEATURES OF ENDOTHELIAL DYSFUNCTION IN EXPERIMENTAL TYPE 2 DIABETES MELLITUS

Abstract

Introduction. Diabetes mellitus (DM) is one of the most acute medical and social problems in modern society. The leading link in the pathogenesis of diabetes is a persistent increase in blood glucose and insulin resistance of target cells, which in turn leads to complications. Endothelial cells are the first to be affected by high blood glucose concentrations. Hyperglycaemia activates protein kinase C, leads to the accumulation of glycosylated proteins, an increase in the content of oxidised plasma lipoproteins, which causes disruption of vascular energy metabolism and endothelial cell damage Materials and Methods. The experimental study was carried out on rats of both sexes of the Wistar line, weighing 180–200 g, aged 3 months. During the experiment, the animals were divided into two groups – 18 rats each: Group I – intact animals; Group II – animals with modelled diabetes mellitus. Results. It has been established that diabetes mellitus increases vasoconstrictor mediators such as endothelin-1 against the background of a decrease in the activity of endothelial NO synthase, which indicates a violation of the physiological synthesis of nitric oxide, and accordingly leads to the development of endothelial dysfunction in the modelled pathological condition. Conclusions. In type 2 diabetes mellitus, a whole cascade of pathological reactions in the vascular endothelium unfolds. As a result, persistent endothelial dysfunction develops, which leads to the fact that the vascular endothelium itself is involved in the pathogenesis of type 2 diabetes and causes a number of other complications.