Experimental defibrination and bothropase: a study on the fibrinolytic mechanism in vivo.
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.
D000347:Afibrinogenemia / Q000139:chemically induced / Q000378:metabolism; D000614:Aminocaproates / Q000494:pharmacology; D000818:Animals; D007611:Aprotinin / Q000494:pharmacology; D004285:Dogs; D005341:Fibrinolysin / Q000378:metabolism; D005342:Fibrinolysis / Q000187:drug effects; D007263:Infusions, Parenteral; D012910:Snake Venoms / Q000494:pharmacology*
D000614:Aminocaproates; D012910:Snake Venoms; D007611:Aprotinin; D005341:Fibrinolysin