Experimental study on hemostatic effects of agacutin, a novel thrombin-like enzyme from Agkistrodon acutus
BU Xiu-yun
Abstract
BU Xiu-yun
Abstract
AIM: To study the hemostatic effects of agacutin in vivo. METHODS: After agacutin was administrated, the indexes on blood coagulation and fibrinogenlysis system were assayed and the hemostatic effect was obtained by observing the mouse tail bleeding time. RESULTS: The intravenous injection of (0.01)-(0.05) (U·kg~(-1)) markedly shortened (44.9)%-(60.5)% of the rabbit blood coagulation time. After administration, the peak effect appeared in 30 min and the effect delayed for 24 h. The rabbit blood fibrinogen concentration and blood viscosity were decreased, which coincided with the effect of shortening of blood coagulation time. Agacutin had no influence on APTT, the platelet count, platelet releasing activity, platelet in vitro aggregation, and euglobulin coagulation time (ECT), but agacutin had a weak fibrinolytic activity. In vivo, the ip administration of (0.5)-(2.0) (U·kg~(-1)) shortened 24%-66% of the mouse tail bleeding time. CONCLUSION: Agacutin causes a higher concentration of soluble fibrin level in vessel and it does not activate prothrombin (II factor) and XIII factor. The hemostatic function is promoted at the wound. In normal vessel, the soluble fibrin does not form insoluble fibrin clot which resulted in thrombosis in vivo.
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AIM: To study the hemostatic effects of agacutin in vivo. METHODS: After agacutin was administrated, the indexes on blood coagulation and fibrinogenlysis system were assayed and the hemostatic effect was obtained by observing the mouse tail bleeding time. RESULTS: The intravenous injection of (0.01)-(0.05) (U·kg~(-1)) markedly shortened (44.9)%-(60.5)% of the rabbit blood coagulation time. After administration, the peak effect appeared in 30 min and the effect delayed for 24 h. The rabbit blood fibrinogen concentration and blood viscosity were decreased, which coincided with the effect of shortening of blood coagulation time. Agacutin had no influence on APTT, the platelet count, platelet releasing activity, platelet in vitro aggregation, and euglobulin coagulation time (ECT), but agacutin had a weak fibrinolytic activity. In vivo, the ip administration of (0.5)-(2.0) (U·kg~(-1)) shortened 24%-66% of the mouse tail bleeding time. CONCLUSION: Agacutin causes a higher concentration of soluble fibrin level in vessel and it does not activate prothrombin (II factor) and XIII factor. The hemostatic function is promoted at the wound. In normal vessel, the soluble fibrin does not form insoluble fibrin clot which resulted in thrombosis in vivo.
Key concepts: Fibrin, In vivo, Coagulation, Fibrinogen, Platelet, Chemistry, Hemostasis, Prothrombin time