Formation of the venous thrombus after venous occlusion in the experimental mouse model of metabolic syndrome

Abstract

Introduction: The metabolic syndrome is considered to be a risk factor for the venous thromboembolism (VTE) as well as arterial thrombosis. Although obesity, hyperglycemia and dyslipidemia are considered to be important triggering factors, it is difficult to evaluate the relationship between VTE and the metabolic syndrome in a clinical study. Furthermore the mechanism of venous thrombosis initiation still remains elusive.

Materials and methods: 20 min clamp of superior mesenteric vein was applied to 7 w, 16 w-old KK-A(y) mouse and 16 w-old B6J mouse (n = 6 in each group), after de-clamp, the view of the mesenteric vein and intestinal submucosal venule were observed by the intravital microscopy.

Results: Massive thrombi formed in the mesenteric vein in 16 w-old KK-A(y) mice, moderate thrombi formation was observed in 7 w-old KK-A(y) mice, while very few thrombi were observed in B6 J mice. The first event in submucosal venule after de-clamp was the adhesion of leukocytes to the endothelium. Subsequently, leukocytes assembled and platelets covered the leukocyte cluster. These leukocyte-platelet aggregates move from the venule to the vein and finally formed a venous thrombus.

Conclusion: Metabolic syndrome is a risk factor for venous thrombosis. Intravital microscopic examination revealed leukocyte and platelet recruitment to the venule in the early stages of venous thrombosis formation.