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La generación de trombina dependiente de plaquetas después de un tratamiento fibrinolítico in vitro
D L Aronson1, P Chang, C M Kessler
1George Washington University Medical Center, Washington, D.C. 20037.
Circulation
|May 1, 1992
Resumen
Los agentes fibrinolíticos como rt-PA pueden activar directamente las plaquetas, aumentando la generación de trombina y potencialmente contribuyendo a la retrombosis. Esto sugiere un efecto plaquetario directo independiente de la activación del plasminógeno.
Área de la Ciencia:
- La bioquímica es la bioquímica.
- Hematología Hematología.
- Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular
Sus antecedentes:
- La terapia fibrinolítica es crucial para el tratamiento de la trombosis, pero está relacionada con la retrombosis.
- La evidencia sugiere que tanto el aumento de la coagulación como la activación plaquetaria contribuyen a este fenómeno.
Objetivo del estudio:
- Investigar los efectos directos de los agentes fibrinolíticos en la activación plaquetaria y la generación de trombina.
- Para determinar si los agentes fibrinolíticos pueden afectar directamente la función plaquetaria independientemente del plasminógeno.
Principales métodos:
- El plasma rico en plaquetas (PRP) y las plaquetas lavadas se incubaron con urokinasa, activador de plasminógeno de tipo tejido recombinante (rt-PA) o plasmina.
- La generación de trombina y los tiempos de coagulación se midieron en PRP y plasma tratados y no tratados.
- Las plaquetas lavadas tratadas con agentes fibrinolíticos se agregaron al plasma pobre en plaquetas para evaluar su apoyo a la generación de trombina.
Principales resultados:
- Los agentes fibrinolíticos aceleraron la generación de trombina y redujeron los tiempos de coagulación en PRP.
- El activador de plasminógeno recombinante de tipo tisular (rt-PA) y la plasmina, pero no la urokinasa, mejoraron la capacidad de las plaquetas lavadas para apoyar la generación de trombina.
- El efecto procoagulante de rt-PA en las plaquetas se observó incluso sin plasminogénesis.
Conclusiones:
- La plasmina aumenta directamente el apoyo plaquetario de la activación de la protrombina.
- El activador de plasminógeno de tipo tisular recombinante (rt-PA) puede afectar directamente a las plaquetas, mejorando la generación de trombina independientemente del plasminógeno.
- Estos hallazgos ponen de relieve un mecanismo de activación plaquetaria directa por agentes fibrinolíticos, lo que podría explicar la retrombosis después de la terapia.
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