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Propiedades contráctiles y actividad de liberación de Ca2+ del retículo sarcoplásmico en cardiomiopatía dilatada
A D'Agnolo1, G B Luciani, A Mazzucco
1Institute of Cardiovascular Surgery, University of Padua, Italy.
Circulation
|February 1, 1992
Resumen
La cardiomiopatía dilatada idiopática muestra proteínas contráctiles normales pero canales anormales de liberación de calcio en el retículo sarcoplásmico. Esto sugiere un papel para el acoplamiento de excitación-contracción en la enfermedad.
Área de la Ciencia:
- Fisiología cardiovascular fisiología cardiovascular.
- Cardiología Molecular Cardiología Molecular
- Biología Muscular Biología Muscular
Sus antecedentes:
- La cardiomiopatía dilatada idiopática (CDI) afecta la función del miocardio.
- El análisis comparativo de la liberación de Ca2+ del retículo sarcoplásmico (SR) y la sensibilidad al calcio del aparato contráctil en los corazones no fallidos e IDC es crucial.
Objetivo del estudio:
- Para comparar la actividad de liberación de Ca2+ de la SR y la sensibilidad al calcio del aparato contráctil en corazones humanos con y sin IDC.
- Investigar el papel del acoplamiento excitación-contracción en la patogénesis de la CID.
Principales métodos:
- Se utilizaron fibras miocárdicas descascaradas químicamente de corazones humanos (sin fallar y IDC).
- Las mediciones de tensión isométrica evaluaron la sensibilidad de Ca2+ del aparato contráctil y la liberación de Ca2+ SR a través del desafío de la cafeína.
- Las fibras se estudiaron en diferentes longitudes de estiramiento (130% y 150% de la longitud de reposo).
Principales resultados:
- No se observó ninguna diferencia significativa en la sensibilidad o la cooperatividad de Ca2+ entre el miocardio normal e IDC a una longitud de reposo del 130%.
- El aumento del estiramiento (150%) aumentó la sensibilidad al Ca2+ en ambos grupos, pero disminuyó el coeficiente de Hill en IDC.
- El umbral de cafeína para la liberación de Ca2+ se elevó notablemente en el IDC, lo que indica una función SR alterada, mientras que la extensión y la velocidad de liberación fueron similares.
Conclusiones:
- Las proteínas contráctiles y reguladoras no se alteran en el IDC.
- Las anomalías en el mecanismo de bloqueo del canal de liberación de Ca2+ de SR sugieren un papel para el acoplamiento de excitación-contracción en la patogénesis de IDC.
- El aumento del umbral de cafeína en el IDC puede deberse a propiedades alteradas de la membrana SR.
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