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http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2540| Título : | Inhibition of the nitric oxide/cyclic guanosine monophosphate pathway limited the cardioprotective effect of post-conditioning in hearts with apical myocardial infarction |
| Creador: | Correa Francisco |
| Nivel de acceso: | Open access |
| Palabras clave : | Animales Guanosina Monofosfato - antagonistas & inhibidores Guanosina Monofosfato - metabolismo Poscondicionamiento Isquémico - métodos Masculino Mitocondrias Cardíacas - efectos de drogas Mitocondrias Cardíacas - metabolismo Mitocondrias Cardíacas - ultraestructura Infarto del Miocardio - metabolismo Infarto del Miocardio - patología Infarto del Miocardio - prevención & control Daño por Reperfusión Miocárdica - metabolismo Daño por Reperfusión Miocárdica -patología Daño por Reperfusión Miocárdica - prevención & control NG-Nitroarginina Metil Éster -farmacología Óxido Nítrico - antagonistas & inhibidores Óxido Nítrico - metabolismo Ratas Ratas Wistar Transducción de Señal - efectos de drogas Transducción de Señal - fisiología Animals Guanosine Monophosphate -antagonists & inhibitors Guanosine Monophosphate - metabolism Ischemic Postconditioning - methods Male Mitochondria, Heart - drug effects Mitochondria, Heart - metabolism Mitochondria, Heart - ultrastructure Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardial Infarction - prevention & control Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - prevention & control NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - antagonists & inhibitors Nitric Oxide - metabolism Rats Rats, Wistar Signal Transduction - drug effects Signal Transduction - physiology Isoproterenol Post-acondicionamiento Lesión por reperfusión CGMP Isoproterenol Post-conditioning Reperfusion injury cGMP |
| Descripción : | Reperfusion damage involves opening of the mitochondrial permeability transition pore (mPTP) and loss of ATP synthesis. Several cardioprotective pathways are activated by ischemic or pharmacological post-conditioning (PC). The mechanisms that are activated by PC in no co-morbidity murine models include: activation of rescue kinases, oxidative stress reduction, glycolytic flux regulation and preservation of ATP synthesis. However, relatively scarce efforts have been made to define whether the efficacy of PC signaling is blunted by risk factors or systemic diseases associated with ischemic heart pathology. Experimental evidence has shown that the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling is a main mechanism activated by PC in hearts without pathological history. In this work we evaluated the participation of the NO pathway, through downstream kinase activation and inhibition of mPTP in hearts with previous infarct. Myocardial infarction was induced with a single dose of isoproterenol (85 mg/kg i.p.) to male Wistar rats. After 24 h, the hearts were mounted into the Langendorff system and subjected to 30 min of ischemia and 60 min of reperfusion. PC consisted of 5 cycles of 30 s of reperfusion/30 s of ischemia, then the hearts were reperfused with or without inhibitors of the NO/cGMP pathway. PC activates the NO/cGMP pathway, as increased cGMP and NO levels were detected in isoproterenol-treated hearts. The cardioprotective effect of PC was abolished with both l-NAME (inhibitor of constitutive NO synthase) and ODQ (inhibitor of soluble guanylate cyclase), whereas the NO donor (DETA-NO) restored cardioprotection even in the presence of l-NAME or ODQ. We also found that mitochondrial structure and function was preserved in PC hearts. We conclude that PC exerts cardioprotection in hearts with previous infarct by maintaining mitochondrial structure and function through NO-dependent pathway. © 2015 Published by Elsevier B.V. |
| Colaborador(es) u otros Autores: | Buelna-Chontal Mabel Chagoya Victoria García-Rivas Gerardo Vigueras Villaseñor Rosa María Pedraza-Chaverri José Ramsés García-Niño Wylly Hernández-Pando Rogelio León-Contreras Juan Carlos Zazueta Cecilia |
| Fecha de publicación : | 2015 |
| Tipo de publicación: | Artículo |
| Formato: | |
| Identificador del Recurso : | 10.1016/j.ejphar.2015.09.018 |
| Fuente: | European Journal of Pharmacology 765():472 - 481 |
| URI : | http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2540 |
| Idioma: | eng |
| Aparece en las colecciones: | Artículos |
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