A Study of the Early Disturbances in Vascular Hemostasis in Experimentally Induced Metabolic Syndrome

Abstract

The unique characteristics of the early changes in vascular haemostasis during the development of metabolic syndrome are still unclear. This study aimed to examine the development of vascular dysfunction in experimentally induced metabolic syndrome. The study used 61 male Wistar rats aged 2.5-3 months. Thirty-two rats were given ad libitum access to 10% fructose dilution for drinking, while the remaining 29 control group rats were not given the fructose dilution. The study period was 8 weeks. We used biochemical, haematological, and statistical methods for investigation. The experimental rats received fructose, and we observed a deteriorating trend in their plasma lipid composition within 2 weeks. At the end of 4 weeks, it had further deteriorated, and it progressively worsened until the end of the experimental period. At the end of 2 weeks, there was significant reduction in the plasma antioxidant activity and rise in the levels of plasma lipid peroxidation products in the experimental rats. This effect persisted throughout the experimental period. At the end of 4 weeks, we observed imbalances in the metabolites; the plasma levels of arachidonic acid peaked by the 8th week; in addition, thromboxane B2 levels rose by 37.3% and 6-keto-prostaglandin F1α levels reduced by 21.8%. This was accompanied by an increase in endothelin-1 and decrease in the total nitric oxide metabolites by 20.2% in the experimental rats. At the end of 2 weeks, there was a reduction in the anticoagulant and fibrinolytic activities of the vessels of the experimental group rats; this effect increased with time. By 4 weeks, the vascular regulation of platelet aggregation in response to collagen, adenosine diphosphate and ristomicin had weakened in the experimental rats. Under experimental conditions of fructose ingestion, there was evident progressive weakening of antiaggregatory, anticoagulative, and fibrinolytic abilities of the vascular endothelium due to the inhibition of the production of prostacyclin, nitric oxide, antithrombin III, and tissue activator plasminogen in the vessels with a simultaneous increase in the body mass of the rats and the development of biochemical abnormalities that were characteristic of metabolic syndrome.