[Pharmacologic influence on secondary generalized fibrinolysis].
Secondary generalized hyperfibrinolysis was induced by thrombin infusion or batroxobin injection in rats. To follow intravascular fibrinolysis quantitatively, an electroimmuno-assay was used for determination of the fibrin degradation products formed. Anticoagulants (heparin, hirudin), antifibrinolytics (EACA, PAMBA, AMCA), and synthetic (APPA) and naturally occurring (aprotinin) protease inhibitors were studied with regard to their influence on secondary fibrinolysis. The potency and duration of action of the antifibrinolytics tested correspond to their antifibrinolytic activity measured in vitro and to their pharmacokinetics. Formation of degradation products is initiated after the appearance of fibrin monomer or fibrin, respectively. Due to their antithrombin action heparin, hirudin, and APPA prevent the thrombin-induced fibrin formation and thus the induction of secondary fibrinolysis. In contrast, formation of fibrin monomers caused by batroxobin is not influenced by thrombin inhibitors so that in this case formation of degradation products is not prevented.
D000818:Animals; D012103:Batroxobin / Q000494:pharmacology; D003435:Crotalid Venoms / Q000494:pharmacology; D005260:Female; D005337:Fibrin / Q000502:physiology; D005340:Fibrinogen / Q000502:physiology; D005342:Fibrinolysis / Q000187:drug effects*; D007700:Kinetics; D010447:Peptide Hydrolases / Q000494:pharmacology; D051381:Rats; D013917:Thrombin / Q000494:pharmacology*
D003435:Crotalid Venoms; D005337:Fibrin; D005340:Fibrinogen; D010447:Peptide Hydrolases; D012103:Batroxobin; D013917:Thrombin
Pharmakologische Beeinflussung der sekundären generalisierten Fibrinolyse.