Influence of the fast-acting inhibitor of plasminogen activator on in vivo thrombolysis induced by tissue-type plasminogen activator in rabbits. Interference of tissue-derived components

The influence of endotoxin-induced elevated plasma levels of the fast-acting inhibitor of plasminogen activator (PA-inhibitor) on thrombolysis was investigated in rabbits with a jugular vein thrombus. Infusion of human tissue-type plasminogen activator (t-PA) produced similar degrees of thrombolysis...

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Detalles Bibliográficos
Autores: Colucci, M. (M.)|||/items/4eda9c08-b77a-450e-b65a-1e4858fda75a, Páramo-Fernández, J.A. (José Antonio)|||/items/8c56baa6-2a43-4836-b91b-4eed15be3c96, Stassen, J.M. (J.M.)|||/items/3106273c-90de-4469-b249-37b42ffa5baf, Collen, D. (D.)|||/items/879361bf-d2c1-4d21-b62e-dd439ac8e527
Tipo de recurso: artículo
Fecha de publicación:1986
País:España
Institución:Universidad de Navarra
Repositorio:Dadun. Depósito Académico Digital de la Universidad de Navarra
Idioma:inglés
OAI Identifier:oai:dadun.unav.edu:10171/22924
Acceso en línea:https://hdl.handle.net/10171/22924
Access Level:acceso abierto
Palabra clave:Fibrinolysis/drug effects
Glycoproteins/pharmacology
Tissue Plasminogen Activator/antagonists & inhibitors
Descripción
Sumario:The influence of endotoxin-induced elevated plasma levels of the fast-acting inhibitor of plasminogen activator (PA-inhibitor) on thrombolysis was investigated in rabbits with a jugular vein thrombus. Infusion of human tissue-type plasminogen activator (t-PA) produced similar degrees of thrombolysis in control and endotoxin-treated rabbits, although no free t-PA could be demonstrated in plasma of endotoxin-treated animals. Infusion of t-PA in an extracorporeal arteriovenous shunt resulted in loss of thrombolytic activity in endotoxin-treated animals but not in control animals. Blood clots superfused in vitro with mixtures of t-PA and normal plasma lysed in contrast to clots superfused with t-PA and PA-inhibitor-rich plasma. However, addition of rabbit lung slices to the plasma surrounding the blood clot, reversed the inhibition of thrombolysis by PA-inhibitor-rich plasma. This indicates that tissue-derived factor(s) are involved in the regulation of in vivo thrombolysis. These hypothetical factor(s) are, however, very unstable in plasma, which has thus far precluded their further characterization.