The role of hemostatic changes in the pathogenesis of diabetic retinopathy

Abstract

Introduction: The paper presents the results of the hemostasis system of rats with experimental diabetic retinopathy.

Material and methods: Experimental studies were performed on white Wistar rats, which were divided into 2 groups: 1^st group – intact animals; 2^nd group – 60 animals with modelling of diabetic retinopathy without correction (control pathology). Аnalysis of the hemostasis system was performed according to the following indicators: plasma recalcification time, activated partial thromboplastin time, prothrombin time, thrombin time, heparin time, thermostable thromboplastin inhibitor, thermolabile thromboplastin inhibitor and fibrinogen level.

Results: Under the conditions of simulated diabetic retinopathy, the time of plasma recalcification was significantly reduced by 1.2 times (p<0.05) compared to intact rats; prothrombin time – 1.4 times (p<0.05); thrombin time – 1.1 times; heparin time – 1.1 times; thermostable thromboplastin inhibitor – 1.0 times; thermolabile thromboplastin inhibitor – 1.5 times (p<0.05), respectively. There was also a significant increase in the level of activated partial thromboplastin time by 1.3 times (p<0.05) compared to the intact group of animals and the level of fibrinogen by 4.9 times (p<0.05), respectively. Such violations of hemostasis at the initial stage of the development of diabetic retinopathy R are associated with inhibition of anticoagulation mechanisms, since the contact phase of hemocoagulation did not change significantly.

On the 120^th day of the experimental studies, the plasma recalcification time decreased by 1.3 times (p<0.05) compared to intact rats; prothrombin time - 1.5 times (р<0.05); thrombin time – 1.3 times (p<0.05); heparin time – 1.2 times (p<0.05); thermostable thromboplastin inhibitor - 1.1 times; thermolabile thromboplastin inhibitor - 2.0 times (p<0.05), respectively. It was established that the activated partial thromboplastin time also increased significantly by 1.4 times (p<0.05) compared to intact rats; there was a 4.0-fold increase in the concentration of fibrinogen (p<0.05), respectively, in intact animals.

Conclusions: DM is characterized by a number of changes in the hemostasis system, which determine the risk of thrombotic complications. One of the main reasons for these changes is: insulin resistance, hyperinsulinemia and insufficient compensation of carbohydrate metabolism. Hypercoagulation in DR conditions is manifested by an increase in the concentration and activity of factors VII and fibrinogen.