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The role of active thrombosis in the pathophysiology of pulmonary embolism is unclear. We tested the hypothesis that venous thrombi significantly increase their thrombotic activity once they embolize into the high-flow circulation of the pulmonary arteries. Thrombotic activity was measured using an immunoassay that measures both fibrinopeptide B (FPB) as well as its most abundant metabolite, des-arginine FPB. Thrombi were formed in the femoral veins of adult dogs. In one group, the thrombi were embolized without anticoagulation. In the second group, heparin (300 units/kg bolus, then 90 units/kg/hour infusion) was administered prior to embolization to prevent subsequent thrombotic activity. Plasma FPB concentrations were significantly suppressed in the heparinized group relative to the non-heparinized group for one hour post-embolization (p = 0.038). We conclude that pulmonary embolization itself causes pre-existing venous thrombi to greatly intensify their thrombotic activity, and that embolization-associated thrombus propagation can be prevented by heparin