Kelen E M, Rosenfeld G, Vainzof M, Machado Z C
Haemostasis. 1978;7(1):35-45. doi: 10.1159/000214230.
Fibrinogen was depleted in dogs injected with a single dose of bothropase even if pretreatment followed by a continuous infusion of antifibrinolytic drugs was performed during defibrination. The activation of the fibrinolytic system as a secondary effect of the defibrination syndrome induced by bothropase injection was blocked completely by aprotinin (Trasylol) but not by EACA. Plasmin activity in spite of the inhibition of plasminogen activator suggests that, either an excess of activator is released in circulation or a plasmin-antiplasmin complex is dissociated by the circulating fibrin, according to the hypothesis of Ambrus and Markus [1], and Back et al. [4] for the mechanism of fibrinolysis in vivo. An experimental model is suggested for the study of the fibrinolytic mechanism in vivo, by the association of defibrinating agents, antivenom and antifibrinolytic drugs.
即使在去纤维蛋白过程中进行了预处理并持续输注抗纤溶药物，注射单剂量博托酶的犬类纤维蛋白原仍会减少。作为博托酶注射诱导的去纤维蛋白综合征的继发效应，纤溶系统的激活被抑肽酶（抑胰肽酶）完全阻断，但氨基己酸（EACA）则不能。尽管纤溶酶原激活物受到抑制，但纤溶酶活性表明，根据安布鲁斯和马库斯[1]以及巴克等人[4]提出的体内纤溶机制假说，要么循环中释放了过量的激活物，要么循环中的纤维蛋白使纤溶酶 - 抗纤溶酶复合物解离。通过联合使用去纤维蛋白剂、抗蛇毒血清和抗纤溶药物，提出了一个用于研究体内纤溶机制的实验模型。
