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La acción aritmogénica de la trombina durante la reperfusión miocárdica a través de la liberación de inositol
A N Jacobsen1, X J Du, K A Lambert
1Cellular Biochemistry Laboratory, Baker Medical Research Institute, Melbourne, Australia.
Circulation
|January 1, 1996
Resumen
Las arritmias de reperfusión dependen de la liberación de inositol 1,4,5-trifosfato (Ins(1,4,5) P3). La trombina y la norepinefrina estimulan la liberación de Ins(1,4,5) P3, lo que desencadena arritmias cardíacas durante la reperfusión.
Área de la Ciencia:
- Cardiología Cardiología.
- La bioquímica es la bioquímica.
- Farmacología Farmacología.
Sus antecedentes:
- La reperfusión cardíaca puede desencadenar arritmias, en parte a través de la estimulación de la norepinefrina de los receptores alfa1-adrenérgicos.
- La liberación de inositol 1,4,5-trifosfato (Ins(1,4,5) P3) está implicada en este proceso.
Objetivo del estudio:
- Para investigar los efectos aritmogénicos de la liberación de Ins(1,4,5) P3 estimulada por la trombina.
- Comprender el papel de Ins(1,4,5) P3 en las arritmias cardíacas inducidas por reperfusión.
Principales métodos:
- Medición de la liberación de Ins(1,4,5) P3 en corazones de rata aislados utilizando cromatografía líquida de alto rendimiento.
- Evaluación de las arritmias cardíacas en corazones de rata con amortiguador perfundido.
- Utilizando corazones empobrecidos con catecolaminas e inhibidores específicos (gentamicina, U-73122) para dilucidar las vías de señalización.
Principales resultados:
- La reperfusión aumentó significativamente los niveles de Ins{1,4,5) P3 en los corazones intactos, pero no en los corazones empobrecidos de catecolaminas.
- La trombina o su péptido agonista restauraron la liberación de Ins(1,4,5) P3 e indujeron arritmias en corazones empobrecidos por catecolaminas.
- La gentamicina y el inhibidor de la fosfolipasa C U-73122 inhibieron la liberación de Ins(1,4,5) P3 inducida por la trombina y las arritmias, mientras que U-73122 no afectó las respuestas inducidas por la norepinefrina.
Conclusiones:
- Las arritmias de reperfusión son críticamente dependientes de la liberación de Ins(1,4,5) P3.
- La trombina contribuye a las arritmias de reperfusión a través de la señalización Ins{1,4,5) P3, distinta de la vía de la norepinefrina.
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