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El curso temporal y el mecanismo de la liberación de catecolaminas miocárdicas durante la isquemia transitoria in
T W Lameris1, S de Zeeuw, G Alberts
1Department of Internal Medicine I, Cardiovascular Research Institute COEUR, Erasmus University Rotterdam, Rotterdam, The Netherlands. TWL@mediaport.org
Circulation
|June 7, 2000
Resumen
La isquemia miocárdica eleva significativamente las catecolaminas en el fluido intersticial miocárdico (MIF), impulsado en parte por la recaptación neuronal inversa. Esto sugiere que los terminales nerviosos simpáticos funcionales persisten incluso después del infarto.
Área de la Ciencia:
- Cardiología Cardiología.
- La neurociencia es la neurociencia.
- Fisiología Fisiología Fisiología.
Sus antecedentes:
- Se observa un aumento de la norepinefrina (NE) en el músculo cardíaco isquémico.
- Investigar los mecanismos de liberación de catecolaminas en el fluido intersticial miocárdico (MIF) durante la isquemia y la reperfusión es crucial.
Objetivo del estudio:
- Determinar la magnitud y el mecanismo de liberación de catecolaminas en MIF durante la isquemia y reperfusión miocárdica.
- Para aclarar el papel de la recaptación neuronal en la liberación de catecolaminas durante la isquemia cardíaca.
Principales métodos:
- Utilizó microdiálisis en cerdos anestesiados para medir las concentraciones intersticiales de catecolaminas.
- Isquemia miocárdica regional inducida por la oclusión de la arteria coronaria descendente anterior izquierda (LAD) durante 60 minutos, seguida de 150 minutos de reperfusión.
- Administración de tiramina durante los últimos 30 minutos de la oclusión para evaluar la capacidad de liberación neuronal.
Principales resultados:
- MIF las concentraciones de norepinefrina, dopamina y epinefrina aumentaron significativamente en la región isquémica durante la oclusión.
- El bloqueo local de absorción-1 redujo la liberación de catecolaminas en más del 50%.
- Los niveles de catecolaminas MIF volvieron a la línea de base durante la reperfusión, y la liberación de NE inducida por tiramina se mantuvo intacta en el tejido infarto.
Conclusiones:
- La isquemia miocárdica causa un aumento sustancial en las catecolaminas MIF, en parte debido a la recaptación neuronal inversa.
- El aumento de epinefrina MIF sugiere una fuente neuronal cardíaca.
- La respuesta conservada de la catecolamina a la tiramina indica terminales nerviosos simpáticos funcionales en el miocardio post-isquémico.
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