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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: pdf
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
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