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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on October 4, 2005; DOI: 10.1124/jpet.105.092023

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Received for publication July 5, 2005.
Revised October 1, 2005.
Accepted for publication October 3, 2005.

Role of hydrogen sulphide in the cardioprotection caused by ischemic preconditioning in the rat heart and cardiac myocytes

Jin-Song Bian 1*, Qian Chen Yong 2, Ting-Ting Pan 1, Zhan-Ning Feng 1, Muhammed Yusuf Ali 3, Shufeng Zhou 1, Philip Keith Moore 1

1 National University of Singapore 2 National Uniersity of Singapore 3 National Univeristy of Singapore

* Address correspondence to: E-mail: phcbjs{at}nus.edu.sg

Abstract

Endogenous H2S is synthesized mainly by cystathionine {gamma}-lyase in the heart. The present study investigated the role of H2S in the cardioprotection induced by ischemic preconditioning. We have examined the effect of endogenous H2S and exogenous application of NaHS (H2S donor) on cardiac rhythm in the isolated rat heart subjected to low-flow ischemia insults as well as cell viability and function in isolated myocytes exposed to simulated ischemia solution. Preconditioning with NaHS (SP) or ischemia (IP) for three cycles (3-min each cycle separated by 5-min of recovery) significantly decreased the duration and severity of ischemia/reperfusion-induced arrhythmias in the isolated heart whilst increasing cell viability and the amplitude of electrically-induced calcium transients after ischemia/reperfusion in the cardiac myocytes. Both IP and SP also significantly attenuated the decreased H2S production during ischemia. Moreover, decreasing endogenous H2S production significantly attenuated the protective effects of IP in the isolated hearts and isolated cardiac myocytes. Blockade of protein kinase C with chelerythrine or bisindolylmaleimide I as well as ATP sensitive K+ (KATP) channel with glibenclamide (a non-selective KATP blocker) and HMR-1098 (a sarcolemmal KATP channel blocker) reversed the cardioprotection induced by SP or IP. However, blockade of mitochondrial KATP channels with 5-hydroxydecanoic acid had no effect on the cardioprotection of SP, suggesting that, unlike the mechanism involved in IP, mitochondrial KATP channels may not play a major role in the cardioprotection of SP. Our findings suggest that endogenous H2S contributes to cardioprotection induced by IP, which may involve PKC and sarcolemmal KATP channels.


Key words: antiarrhythmia agents, arrhythmia, calcium, cardiac myocytes, ischemia, signal transduction




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