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http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2781| Título : | Ru(360), a specific mitochondrial calcium uptake inhibitor, improves cardiac post-ischaemic functional recovery in rats in vivo. |
| Creador: | García Rivas G de J |
| Nivel de acceso: | Open access |
| Palabras clave : | Aconitato Hidratasa - Metabolismo Animales Presión Sanguínea - Efectos de drogas Calcio - Metabolismo Bloqueadores de los Canales de Calcio -metabolismo Bloqueadores de los Canales de Calcio - Farmacologia Bloqueadores de los Canales de Calcio - Uso terapeutico Canales de Calcio - Efectos de drogas Canales de Calcio metabolismo Respiración de la Célula - efectos de drogas Circulación Coronaria - efectos de drogas Ciclosporina - farmacología Relación Dosis-Respuesta a Droga Electrocardiografía Frecuencia Cardíaca - Efectos de drogas Masculino Mitocondrias Cardíacas - Metabolismo Proteínas de Transporte de Membrana Mitocondrial - Efectos de drogas Proteínas de Transporte de Membrana Mitocondrial - Metabolismo Reperfusión Miocárdica - Efectos adversos Daño por Reperfusión Miocárdica - Terapia de drogas Daño por Reperfusión Miocárdica - metabolism Daño por Reperfusión Miocárdica - fisiopatología Miocitos Cardíacos - efectos de drogas Miocitos Cardíacos - metabolismo Ratas wistar Compuestos de Rutenio - metabolismo Compuestos de Rutenio - farmacología Compuestos de Rutenio - uso terapeutico Rojo de Rutenio - farmacología Factores de Tiempo Fibrilación Ventricular - metabolismo Fibrilación Ventricular - prevención y control Aconitate Hydratase - metabolism Animals Blood Pressure - drug effects Calcium - metabolism Calcium Channel Blockers - metabolism Calcium Channel Blockers - pharmacology Calcium Channel Blockers - therapeutic use Calcium Channels - drug effects Calcium Channels - metabolism Cell Respiration - drug effects Coronary Circulation - drug effects Cyclosporine -pharmacology Dose-Response Relationship, Drug Electrocardiography Heart Rate - drug effects Male Mitochondria, Heart - drug effects Mitochondria, Heart - metabolism Mitochondrial Membrane Transport Proteins - drug effects Mitochondrial Membrane Transport Proteins - metabolism Myocardial Reperfusion -adverse effects Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion injury - metabolism Myocardial Reperfusion Injury - physiopathology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Rats, Wistar Ruthenium Compounds - metabolism Ruthenium Compounds - pharmacology Ruthenium Compounds - therapeutic use Ruthenium Red - pharmacology Time Factors Ventricular Fibrillation - metabolism Ventricular Fibrillation - prevention & control mitocondrias lesión por reperfusión uniporter de calcio Ru360 poro de transición de permeabilidad arritmias calcio, sobrecarga mitochondria reperfusion injury calcium uniporter Ru360 permeability transition pore arrhythmias calcium overload |
| Descripción : | The mitochondrial permeability transition pore (mPTP), an energy-dissipating channel activated by calcium, contributes to reperfusion damage by depolarizing the mitochondrial inner membrane potential. As mitochondrial Ca(2+) overload is a main inductor of mPTP opening, we examined the effect of Ru(360), a selective inhibitor of the mitochondrial calcium uptake system against myocardial damage induced by reperfusion in a rat model. EXPERIMENTAL APPROACH: Myocardial reperfusion injury was induced by a 5-min occlusion of the left anterior descending coronary artery, followed by a 5-min reperfusion in anaesthetized open-chest rats. We measured reperfusion-induced arrhythmias and functions indicative of unimpaired mitochondrial integrity to evaluate the effect of Ru(360) treatment. KEY RESULTS: Reperfusion elicited a high incidence of arrhythmias, haemodynamic dysfunction and loss of mitochondrial integrity. A bolus intravenous injection of Ru(360) (15-50 nmol kg(-1)), given 30-min before ischaemia, significantly improved the above mentioned variables in the ischaemic/reperfused myocardium. Calcium uptake in isolated mitochondria from Ru(360)-treated ventricles was partially diminished, suggesting an interaction of this compound with the calcium uniporter. CONCLUSIONS AND IMPLICATIONS: We showed that Ru(360) treatment abolishes the incidence of arrhythmias and haemodynamic dysfunction elicited by reperfusion in a whole rat model. Ru(360) administration partially inhibits calcium uptake, preventing mitochondria from depolarization by the opening of the mPTP. We conclude that myocardial damage could be a consequence of failure of the mitochondrial network to maintain the membrane potential at reperfusion. Hence, it is plausible that Ru(360) could be used in reperfusion therapy to prevent the occurrence of arrhythmia |
| Colaborador(es) u otros Autores: | Carvajal K Correa F Zazueta C. |
| Fecha de publicación : | 2006 |
| Tipo de publicación: | Artículo |
| Formato: | |
| Identificador del Recurso : | 10.1038/sj.bjp.0706932 |
| Fuente: | British Journal of Pharmacology 149(7):829-837 |
| URI : | http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2781 |
| Idioma: | eng |
| Aparece en las colecciones: | Artículos |
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