Radiologic Classification of Iliac Vein Compression and Patterns of Pelvic Collateralization in Patients with Chronic Venous Disease.

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thrombomodulin (TM), plays an integral role in clot formation by catalyzing the conversion of fibrinogen to fibrin. Plasmin, which is formed by the action of urokinase and tissue plasminogen activator (uPA and tPA), is responsible for the enzymatic degradation of the fibrin clot, a process known as fibrinolysis. The goal of this study was to determine the thrombotic reactivity of the pulmonary artery and iliac vein endothelial beds. Methods: Human iliac vein endothelial cells (HIVEC) and human pulmonary artery endothelial cells (HPAEC) were incubated at 37 C in the presence or absence of thrombin (1 nM, 10 nM, 25 nM, and 100 nM) for 24 hours. Plasminogen activator inhibitor-1 (PAI-1), uPA, tPA, EPCR, PAR-1, and TM expression in cell lysates were evaluated by Western blot analysis. Results: While thrombin had no effect on the expression of uPA in HPAEC, there was a w20% decrease in uPA expression in HIVEC in the presence of both 1 nM and 100 nM thrombin. Similarly, when tPA expression was examined, there was no change in HPAEC and a marked increase in HIVEC in response to thrombin. In contrast, thrombin stimulation caused a decrease in PAI-1 expression in HPAEC while having no effect on HIVEC. There was no change in EPCR expression in HPAEC; however, after stimulation with 25 nM and 100 nM thrombin, there was >20% decrease in expression of EPCR in HIVEC. HPAEC demonstrated decreased expression of PAR1 in the presence of 25 nM and 100 nM thrombin, and, in contrast, an almost 40% increase in PAR1 expression was observed in HIVEC. Thrombin produced no change in HIVEC recombinant TM expression; however, 10 nM and 100 nM thrombin produced >20% increased expression of recombinant TM in HPAEC. In addition, there was also w20% increase in the expression of pre-cursor TM in both HPAEC and HIVEC after stimulation with 25 nM thrombin. Conclusions: Endothelial cells from the deep vein and pulmonary artery venous beds differentially express markers of the fibrinolytic and coagulation pathways, and this variance in expression may play a role in the thrombotic reactivity of these vascular beds. This data may aide in the prevention and treatment of patients with pulmonary emboli.