Summary

Deep vein thrombosis (DVT) occurs with high prevalence in associationwith a number of risk factors, including major surgery,trauma, obesity, bed rest (>5 days), cancer, a previous history ofDVT,and several predisposing prothrombotic mutations.A novelmurine model of DVT was developed for applications to preclinicalstudies of transgenically constructed prothromboticlines and evaluation of new antithrombotic therapies.A transientdirect-current electrical injury was induced in the common femoralvein of adult C57Bl/6 mice. A non-occlusive thrombusgrew, peaking in size at 30 min, and regressing by 60 min, as revealedby histomorphometric volume reconstruction of theclot. Pre-heparinization greatly reduced clot formation at 10, 30, and 60 min (p<0.01 versus non-heparinized). Homozygous FactorVLeiden mice (analogous to the clinical FactorV Leiden prothromboticmutation) on a C57Bl/6 background had clot volumesmore than twice those of wild-types at 30 min(0.121±0.018 mm3 vs. 0.052±0.008 mm³ , respectively; p<0.01).Scanning electron microscopy revealed a clot surface dominatedby fibrin strands, in contrast to arterial thrombi which showed aplatelet-dominated structure.This new model of DVT presentsa quantifiable approach for evaluating thrombosis-related murinetransgenic lines and for comparatively evaluating new pharmacologicapproaches for prevention of DVT