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-alpha and
PKC-epsilon but not that of PKC-delta, Akt, and
endothelial nitric oxide synthase (eNOS). These data suggest that endogenous H2S contributes partially to the cardioprotection of IPostC via stimulating PKC-alpha and
PKC-epsilon. 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 microM) or PKC with
chelerythrine (10 microM) 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.