An in vivo examination of the differences between rapid cardiovascular collapse and prolonged hypotension induced by snake venom.

摘要: We investigated the cardiovascular effects of venoms from seven medically important species snakes: Australian Eastern Brown snake (Pseudonaja textilis), Sri Lankan Russell’s viper (Daboia russelii), Javanese (D. siamensis), Gaboon (Bitis gabonica), Uracoan rattlesnake (Crotalus vegrandis), Carpet (Echis ocellatus) and Puff adder arietans), identified two distinct patterns effects: i.e. rapid collapse prolonged hypotension. P. textilis (5 µg/kg, i.v.) E. ocellatus (50 µg/kg, induced (i.e. within 2 min) in anaesthetised rats. (20 mg/kg, i.m.) caused 10 min. D. russelii (100 µg/kg, siamensis ‘prolonged hypotension’, characterised by a persistent decrease blood pressure with recovery. venom (50 mg/kg 100 mg/kg, also A priming dose (2 µg/kg, prevented i.v.), but had no significant effect on subsequent addition (1 mg/kg, i.v). Two doses (1 µg/kg, i.v.). B. gabonica, C. vegrandis arietans (all at 200 µg/kg, mild transient Artificial respiration hypotension not venom. (0.001–1 μg/ml) concentration-dependent relaxation (EC50 = 82.2 ± 15.3 ng/ml, Rmax = 91 ± 1%) pre-contracted mesenteric arteries. In contrast, (1 µg/ml) only produced maximum relaxant 27 ± 14%, suggesting that is unlikely to be due peripheral vasodilation. The prevention collapse, ‘priming’ venom, supports role for depletable endogenous mediators this phenomenon.