1040 is regulated at two levels: localised plasminogen activation action at the concentrations obtained in vivo) reduced the frethe fibrin surface and protection of the formed plasmin from quency and severity of episodes of joint bleeding and ecchymoses is in perfect agreement with this hypothesis. circulating x2 antiplasmin. The lysine-binding sites in the plasThese experiments do rule out the existence of a specific inminogen molecule seem to play a key role in these regulations since they mediate the interaction with fibrin on the one hand hibitor to plasminogen activator in the blood. The evidence on and the fast inhibition of plasmin by a2 antiplasmin on the which its existence is postulated can however be interpreted in other. When fibrin is formed, a small amount of plasminogen terms of already known molecular interactions. is specifically bound to it by way of its lysine-binding sites. The scope of this discussion goes beyond the academic interest of explaining a single patient’s bleeding tendency. A better Plasminogen activator present in the blood or released from the vascular endothelium is adsorbed on the fibrin surface and understanding of the molecular mechanism of fibrinolysis efficiently activates the adsorbed plasminogen. The formed might provide us with more rational approaches to its theraplasmin bound to fibrin is partly protected from circulating peutic enhancement than the largely empirical approach to Cl2-antiplasmin, whereas plasmin released from the fibrin surthrombolysis used to date. face is rapidly and irreversibly neutralised by

Vidarabine monophosphate in viral encephalitis.

1040 is regulated at two levels: localised plasminogen activation action at the concentrations obtained in vivo) reduced the frethe fibrin surface and...
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