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Endogenous hydrogen sulphide mediates the cardioprotection induced by ischemic postconditioning

Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore

Submitted 10 March 2008 ; accepted in final form 22 July 2008

The present study aimed to investigate the role of hydrogen sulphide (H₂S) in the cardioprotection induced by ischemic postconditioning and to examine the underlying mechanisms. Cardiodynamics and myocardial infarction were measured in isolated rat hearts. Postconditioning with six episodes of 10-s ischemia (IPostC) significantly improved cardiodynamic function, which was attenuated by the blockade of endogenous H₂S production with D-L-propargylglycine. Moreover, IPostC significantly stimulated H₂S synthesis enzyme activity during the early period of reperfusion. However, D-L-propargylglycine only attenuated the IPostC-induced activation of PKC- and PKC- but not that of PKC-, Akt, and endothelial nitric oxide synthase (eNOS). These data suggest that endogenous H₂S contributes partially to the cardioprotection of IPostC via stimulating PKC- and PKC-. Postconditioning with six episodes of a 10-s infusion of NaHS (SPostC) or 2 min continuous NaHS infusion (SPostC2) stimulated activities of Akt and PKC, improved the cardiodynamic performances, and reduced myocardial infarct size. The blockade of Akt with LY-294002 (15 µM) or PKC with chelerythrine (10 µM) abolished the cardioprotection induced by H₂S postconditioning. SPostC2, but not SPostC, also additionally stimulated eNOS. We conclude that endogenous H₂S contributes to IPostC-induced cardioprotection. H₂S postconditioning confers the protective effects against ischemia-reperfusion injury through the activation of Akt, PKC, and eNOS pathways.

Akt; protein kinase C; hydrogen sulphide; endothelial nitric oxide synthase

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