Endogenous hydrogen sulfide regulation of myocardial injury induced by isoproterenol.

Authors: Geng B (1,2) , Chang L (2,3) , Pan C (3) , Qi Y (1,2) , Zhao J (1,2) , Pang Y (1,2) , Du J (4) , Tang C (1,2)
(1) Institute of Cardiovascular Research, Peking University First Hospital (2) Reference Laboratory of the Ministry of Education on Molecular Cardiology, Health Science Center (3) Department of Physiology, Peking University Health Science Center (4) Department of Pediatrics, Peking University First Hospital
Source: Biochem Biophys Res Commun. 2004 Jun 4;318(3):756-63.
DOI: 10.1016/j.bbrc.2004.04.094 Publication date: June 4, 2004 E-Publication date: Not specified Availability: abstract Copyright: © 2004 Elsevier Inc. All rights reserved.
Language: English Countries: Not specified Location: Not specified Correspondence address: Tang C : tangchaoshu@263.net.cn


Article abstract

Previous work has shown that the endogenous cystathionine gamma-synthase (CSE)/hydrogen sulfide (H(2)S) pathway participates in the regulation of cardiac contraction. We hypothesized that the pathway might participate in the pathophysiological regulation of ischemic heart disease. Isoproterenol injection of rat hearts induced a myocardial ischemic injury model, with reduced myocardial and plasma H(2)S levels, decreased CSE activity, and upregulated CSE gene expression. Exogenous administration of the H(2)S donor NaHS reduced the mortality rate; increased left-ventricular pressure development and left-ventricular-end systolic pressure; and decreased left-ventricular-end diastolic pressure (LVEDP) and subendocardial necrosis, capillary dilatation, leukocytic infiltration, fibroblast swelling, and fibroblastic hyperplasia. As well, production of lipid peroxidation, including myocardial malondialdehyde (MDA), and plasma MDA and conjugated diene, was reduced. Oxidative stress injury is an important mechanism of isoproterenol-induced myocardial injury. In vitro experiments revealed that NaHS might antagonize myocyte MDA production by oxygen-free radicals and that NaHS directly scavenged hydrogen peroxide and superoxide anions. Our results suggest that the endogenous CSE/H(2)S pathway contributes to the pathogenesis of isoproterenol-induced myocardial injury. Administration of exogenous H(2)S effectively protects myocytes and contractile activity, at least by its direct scavenging of oxygen-free radicals and reducing the accumulation of lipid peroxidations.

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