IN-VIVO EFFECT OF A THROMBIN-LIKE ENZYME ON PLATELET PLUG FORMATION INDUCED IN MESENTERIC MICROVESSELS OF MICE

Ancrod caused defibrinogenation and exhibited ex vivo antiplatelet act ivity in experimental rabbits. In this study, platelet thrombus was in duced by irradiation of the mesenteric microvessels with filtered ligh t 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 int ravenously infused. At these doses, ancrod depleted plasma fibrinogen and displayed ex vivo antiplatelet aggregation induced by collagen. An crod (1 U/kg) prolonged the occlusion time about 2.1 folds (from contr ol 103.2+/-17.0 to 211.2+/-26.3 seconds) with a duration longer than 6 0 min. On the other hand, PGI(2) briefly prolonged the occlusion time about 1.5 folds when it was given by continuous infusion (250-500 ng/k g/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 tre atment of venous thrombosis and possibly in prevention of arterial thr ombosis.