title: Hydrogen sulfide improves cardiomyocytes electrical remodeling post ischemia/reperfusion injury in rats.
abstract: Hydrogen sulfide (H2S), produced by cystanthionine-γ-lysase (CSE) in the cardiovascular system, is an endogenous gaseous mediator exerting pronounced physiological effects as the third gasotransmitter in addition to nitric oxide (NO) and carbon monoxide (CO). Accumulating evidence indicated that H2S could mediate the cardioprotective effects in myocardial ischemia model. Ventricular arrhythmia is the most important risk factor for cardiac mortality and sudden death after acute myocardial infarction (AMI). The potential impact of H2S on cardiomyocytes electrical remodeling post ischemic insult is not fully explored now. Present study investigated the role of H2S on cardiomyocytes electrical remodeling in rats with ischemia/reperfusion injury. H2S concentration was reduced and arrhythmia score was increased in this model. CSE mRNA level was also upregulated in the ischemic myocardium. Exposure to exogenous NaHS reduced the action potential duration (APD), inhibited L-type Ca(2+) channels and activated K(ATP) channels in cardiomyocytes isolated from ischemic myocardium Exogenous H2S application improves electrical remodeling in cardiomyocytes isolated from ischemic myocardium. These results indicated that reduced H2S level might be linked to ischemia/reperfusion induced arrhythmias.
authors.affiliation: Department of Cardiovascular Diseases, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200092, China.
authors.forename: Ying-Gang
authors.initials: YG
authors.lastname: Sun
authors.affiliation: Department of Anatomy and Physiology, Shanghai Institute of Health Science Shanghai 201318, China.
authors.forename: Xin-Yan
authors.initials: XY
authors.lastname: Wang
authors.affiliation: Department of Cardiovascular Diseases, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200092, China.
authors.forename: Xiu
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Cardiovascular Diseases, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200092, China.
authors.forename: Cheng-Xing
authors.initials: CX
authors.lastname: Shen
authors.affiliation: Department of Cardiovascular Diseases, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai 200092, China.
authors.forename: Yi-Gang
authors.initials: YG
authors.lastname: Li
mesh_terms: D000818:Animals; D064752:Atrial Remodeling / Q000187:drug effects* / Q000502:physiology; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006862:Hydrogen Sulfide / Q000378:metabolism* / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D006862:Hydrogen Sulfide
keywords: CSE; Hydrogen sulfide; KATP channels; L-type Ca2+ channels; action potential duration; ischemia/reperfusion