Abstract

The aim of the study was to analyze changes in erythrocyte diphosphoglycerate levels and Willebrand factor in the development of hypoxia and endothelial dysfunction in experimental diabetic retinopathy. The study was performed on white Wistar rats weighing 180-200 g. Our results indicate the development of hypoxia on the 30th day of development of experimental diabetic retinopathy with subsequent progression of pathological changes on the 60th and 180th day of the study, as evidenced by the decrease level of 2,3 diphosphoglycerate of erythrocytes in the 2nd group (p <0,001). The most pronounced increase in the studied marker of hypoxia was detected in the 3rd stage of the experiment (p <0,001). As a result of our study, a violation of the structural and functional state of the endothelium in experimental diabetic retinopathy was proved, as evidenced by an increase in the level of Willeband factor in group 2 (p <0.001), most pronounced in stage 3. The most pronounced increase in the level of Willebrand factor was detected in the 3rd stage of the experiment (p <0.001). Analyzing the data obtained, we can say that there is a relationship between the development of hypoxia and endothelial dysfunction in the pathogenesis of experimental diabetic retinopathy.

Highlights

  • As noted, diabetes is characterized by a number of complications that can lead to disability, complete disability and even premature death

  • In the group in which diabetic retinopathy was simulated without further correction already at the 1st stage revealed an increase in the level of Willebrand factor by 19.66% compared with data from intact animals (p

  • Our results indicate the development of hypoxia on the 30th day of experimental diabetic retinopathy with subsequent progression of pathological changes on the 60th and 180th day of the study, as evidenced by a decrease in 2.3 levels of erythrocyte diphosphoglycerate in the 2nd group (p

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Summary

Introduction

Diabetes is characterized by a number of complications that can lead to disability, complete disability and even premature death. Mortality from diabetes reduces the lives of patients by 1214 years due to vascular accidents, which were recorded in 75-80% of cases. The main cause of death in this pathology are vascular complications: nephropathy, neuropathy, retinopathy, amputation, stroke, cardiovascular disease, in the pathogenesis of which a key swarm is played by hyperglycemia and related metabolic effects [2]. Complications that occur in the late stages of diabetes are divided into micro- and macroangiopathy, the formation of which in diabetes determines the prognosis for quality and life expectancy of patients, so we can say that "diabetes begins as a metabolic disease" and ends as a vascular catastrophe» [3]. It was determined that the initial morphological signs of the studied pathological condition are endothelial cell proliferation, thinning of the basement membrane and loss of pericytes, which in turn leads to aneurysms and violation of vascular capillary diameter and hemodynamics [11, 12]

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