Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.yjmcc.2005.10.003
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dc.titleEndogenous hydrogen sulfide contributes to the cardioprotection by metabolic inhibition preconditioning in the rat ventricular myocytes
dc.contributor.authorPan, T.-T.
dc.contributor.authorFeng, Z.-N.
dc.contributor.authorLee, S.W.
dc.contributor.authorMoore, P.K.
dc.contributor.authorBian, J.-S.
dc.date.accessioned2011-09-29T05:54:36Z
dc.date.available2011-09-29T05:54:36Z
dc.date.issued2006
dc.identifier.citationPan, T.-T., Feng, Z.-N., Lee, S.W., Moore, P.K., Bian, J.-S. (2006). Endogenous hydrogen sulfide contributes to the cardioprotection by metabolic inhibition preconditioning in the rat ventricular myocytes. Journal of Molecular and Cellular Cardiology 40 (1) : 119-130. ScholarBank@NUS Repository. https://doi.org/10.1016/j.yjmcc.2005.10.003
dc.identifier.issn00222828
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/27277
dc.description.abstractThe possible role of hydrogen sulfide (H2S) in cardioprotection was investigated in isolated rat ventricular myocytes exposed to severe metabolic inhibition (MI) in glucose-free buffer containing 2-deoxy-D-glucose (2-DOG), an inhibitor of glycolysis. Pretreatment (30:min) with NaHS (a H 2S donor) at concentrations of 10-5 to 10-4 mol/L caused a concentration related increase in cell viability and the ratio of rod-shaped cells. A time course study showed that NaHS-induced cardioprotection occurred in 2 time windows (~1:h and 16-28:h). To observe whether endogenous H2S may be involved in the delayed cardioprotection response of IP, DL-propargylglycine (PAG) and β-cyano-L-alanine (BCA; two inhibitors of H2S biosynthesis) were used. Both drugs significantly attenuated the cardioprotection produced by MI using cell viability, cellular injury index, and electrically-induced [Ca2+]i transients as end-points. These data suggest that endogenous H2S plays an important role in the cardioprotection following MI preconditioning. In an attempt to determine the mechanism of the cardioprotective effect of H2S, we examined the effect of blocking KATP channels with glibenclamide (a non-selective KATP channel blocker), 5-hydroxydecanoic acid (5-HD, a mitochondrial KATP blocker), and HMR-1098 (a sarcolemmal KATP blocker). The cardioprotective effects of NaHS were significantly attenuated by glibenclamide and HMR-1098 treatment but not by 5-HD. Inhibition of NO production with L-NG nitroarginine methyl ester (L-NAME) also attenuated the cardioprotection of NaHS. In conclusion, our findings provide the first evidence that H2S may protect the heart most probably by activating sarcolemmal KATP channels and/or provoking NO release and the cardioprotective effects of metabolic ischemic preconditioning is, at least partially, mediated by endogenous H2S. © 2005 Elsevier Ltd. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.yjmcc.2005.10.003
dc.sourceScopus
dc.subjectATP-sensitive potassium channels
dc.subjectCardioprotection
dc.subjectIntracellular calcium
dc.subjectMyocardial ischemia
dc.subjectNitric oxide
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.1016/j.yjmcc.2005.10.003
dc.description.sourcetitleJournal of Molecular and Cellular Cardiology
dc.description.volume40
dc.description.issue1
dc.description.page119-130
dc.identifier.isiut000234867700015
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