title: Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function.
abstract: The recent discovery that hydrogen sulfide (H(2)S) is an endogenously produced gaseous second messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential of H(2)S as a cardioprotective agent. In the current study, we demonstrate that the delivery of H(2)S at the time of reperfusion limits infarct size and preserves left ventricular (LV) function in an in vivo model of myocardial ischemia-reperfusion (MI-R). This observed cytoprotection is associated with an inhibition of myocardial inflammation and a preservation of both mitochondrial structure and function after I-R injury. Additionally, we show that modulation of endogenously produced H(2)S by cardiac-specific overexpression of cystathionine gamma-lyase (alpha-MHC-CGL-Tg mouse) significantly limits the extent of injury. These findings demonstrate that H(2)S may be of value in cytoprotection during the evolution of myocardial infarction and that either administration of H(2)S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.
authors: Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
authors: John W
authors: JW
authors: Elrod
authors: John W
authors: JW
authors: Calvert
authors: Joanna
authors: J
authors: Morrison
authors: Jeannette E
authors: JE
authors: Doeller
authors: David W
authors: DW
authors: Kraus
authors: Ling
authors: L
authors: Tao
authors: Xiangying
authors: X
authors: Jiao
authors: Rosario
authors: R
authors: Scalia
authors: Levente
authors: L
authors: Kiss
authors: Csaba
authors: C
authors: Szabo
authors: Hideo
authors: H
authors: Kimura
authors: Chi-Wing
authors: CW
authors: Chow
authors: David J
authors: DJ
authors: Lefer
mesh_terms: D000818:Animals; D017209:Apoptosis; D004452:Echocardiography / Q000379:methods; D006352:Heart Ventricles / Q000473:pathology; D006862:Hydrogen Sulfide / Q000737:chemistry / Q000494:pharmacology*; D007249:Inflammation; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology*; D009206:Myocardium / Q000737:chemistry / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D010101:Oxygen Consumption; D015427:Reperfusion Injury; D019210:Troponin I / Q000378:metabolism
chemical_list: D019210:Troponin I; D006862:Hydrogen Sulfide