In vivo effects of the purified thrombin-like and anticoagulant principles of Agkistrodon acutus (Hundred pace snake) venom

Abstract

The thrombin-like enzyme of Agkistrodon acutus venom caused a marked prolongation of whole blood coagulation time and one-stage plasma prothrombin time and a marked decrease of fibrinogen level, while no significant change in the two-stage plasma prothrombin level was detected. The retardation of blood clotting by the thrombin-like enzyme was chiefly due to the decrease of plasma fibrinogen level. The thrombin-like enzyme did not cause significant change in blood pressure, heart rate, EKG or respiration at a defibrinating dose (0·1 mg/kg, i.v.). It also did not induce platelet aggregation. Fibrin formed by the thrombin-like enzyme was not cross-linked. The thrombin-like enzyme could further digest the α-chain of fibrin and the fibrin formed by this enzyme was more susceptible to plasmin degradation than fibrin formed by thrombin. The anticoagulant principle of Agkistrodon acutus venom caused a marked, but transient prolongation of whole blood coagulation time and one-stage plasma prothrombin time with no significant change in the two-stage plasma prothrombin level or plasma fibrinogen level. Combining these results with our previous in vitro findings, it is concluded that the retardation of blood clotting by the anticoagulant principle might be due to the interference in the interaction between prothrombin and its activation factors. The anticoagulant principle did not affect platelet aggregation induced by ADP. It also did not cause significant change in blood pressure, heart rate, EKG or respiration at an i.v. dose of 1–10 mg/kg.