title: Exogenous hydrogen sulfide postconditioning protects isolated rat hearts against ischemia-reperfusion injury.
abstract: Hydrogen sul fi de (H2S) is an endogenous gaseous mediator, produced by cystanthionine-gamma-lysase (CSE) in the cardiovascular system. Hydrogen sulfide given before ischemia can decrease myocardial ischemia and reperfusion injury. The present study investigated: (1) if hydrogen sulfide given at early reperfusion could decrease myocardial ischemia and reperfusion injury; (2) if the protective effects of hydrogen sulfide were related to mitochondrial ATP-sensitive K+ (KATP) channels opening. In isolated rat heart model, treatment of heart with NaHS (H2S donor) at the onset of reperfusion resulted in a concentration-dependent limitation of infarct size and creatine kinase release. The optimal NaHS concentration for cardioprotection is 1 microM. The cardioprotective effects of NaHS (1, 10 microM) were comparable to those of ischemic postconditioning. The KATP channels blocker, Glibenclamide or 5-hydroxydecanoate, reversed the cardioprotective effects of NaHS. The datum provided further evidence that exogenous H2S postconditioning protected rat heart against ischemia and reperfusion injury. Mitochondrial KATP channel opening is implicated in the postconditioning of H2S.
authors.affiliation: Department of Anesthesiology, the First Affiliated Hospital, China Medical University, Shenyang, 110001, Liaoning Province, China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Ji
authors.forename: Qing-feng
authors.initials: QF
authors.lastname: Pang
authors.forename: Gang
authors.initials: G
authors.lastname: Xu
authors.forename: Li
authors.initials: L
authors.lastname: Wang
authors.forename: Jun-ke
authors.initials: JK
authors.lastname: Wang
authors.forename: Yin-ming
authors.initials: YM
authors.lastname: Zeng
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002021:Buffers; D003326:Coronary Circulation / Q000187:drug effects; D003402:Creatine Kinase / Q000378:metabolism; D003652:Decanoic Acids / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005905:Glyburide / Q000494:pharmacology; D006321:Heart / Q000187:drug effects*; D006334:Heart Function Tests; D006339:Heart Rate / Q000187:drug effects; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D006880:Hydroxy Acids / Q000494:pharmacology; D066298:In Vitro Techniques; D054086:KATP Channels / Q000187:drug effects; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D002021:Buffers; D003652:Decanoic Acids; D006880:Hydroxy Acids; D054086:KATP Channels; C052853:5-hydroxydecanoic acid; D003402:Creatine Kinase; D005905:Glyburide; D006862:Hydrogen Sulfide