Endogenous hydrogen suiphide mediates the cardioprotection induced by ischemic postconditioning.

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-α and PKC-ε but not that of PKC-δ, Akt, and endothelial nitric oxide synthase (eNOS). These data suggest that endogenous H₂S contributes partially to the cardioprotection of IPostC via stimulating PKC-α and PKC-ε. Postconditioning with six episodes of a 10-s infusion of NaHS (SPostC) or 2 min continuous Na}IS 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 nM) 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. [ABSTRACT FROM AUTHOR]