HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 295/3/H1330    most recent 00244.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Yong, Q. C. Articles by Bian, J.-S. PubMed PubMed Citation Articles by Yong, Q. C. Articles by Bian, J.-S.

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