Ancrod caused defibrinogenation and exhibited ex vivo antiplatelet activity in experimental rabbits. In this study, platelet thrombus was induced by irradiation of the mesenteric microvessels with filtered light in mice pretreated with fluorescein sodium intravenously. Ancrod (0.5-2 U/kg) dose-dependently, significantly prolonged the time lapse of inducing platelet plug formation in mesenteric venules when it was intravenously infused. At these doses, ancrod depleted plasma fibrinogen and displayed ex vivo antiplatelet aggregation induced by collagen. Ancrod (1 U/kg) prolonged the occlusion time about 2.1 folds (from control 103.2 +/- 17.0 to 211.2 +/- 26.3 seconds) with a duration longer than 60 min. On the other hand, PGI2 briefly prolonged the occlusion time about 1.5 folds when it was given by continuous infusion (250-500 ng/kg/min). Heparin (100-250 U/kg) had no significant effect in this model. Therefore, ancrod may be used as a therapeutic agent not only in treatment of venous thrombosis and possibly in prevention of arterial thrombosis.