Exogenous hydrogen sulfide postconditioning protects isolated rat hearts against ischemia-reperfusion injury

被引：117

作者：

Ji, Yong ^{[1
,2
]}

Pang, Qing-feng ^{[3
]}

Xu, Gang ^{[2
]}

Wang, Li ^{[2
]}

Wang, Jun-ke ^{[1
]}

Zeng, Yin-ming ^{[1
,2
]}

机构：

[1] China Med Univ, Affiliated Hosp 1, Dept Anesthesiol, Shenyang 110001, Liaoning Prov, Peoples R China

[2] Jiangsu Inst Anesthesiol, Key Anesthesiol Lab Jiangsu Prov, Xuzhou 221004, Jiangsu Prov, Peoples R China

[3] Nanjing Med Univ, Dept Pharmacol, Nanjing 210029, Jiangsu Prov, Peoples R China

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2008年 / 587卷 / 1-3期

基金：

中国国家自然科学基金;

关键词：

hydrogen sulfide; postconditioning; ischemia-reperfusion; K-ATP channel;

D O I：

10.1016/j.ejphar.2008.03.044

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Hydrogen sulfide (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+ (K-ATP) 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 mu M. The cardioprotective effects of NaHS (1, 10 mu M) 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 K-ATP channel opening is implicated in the postconditioning of H2S (c) 2008 Elsevier B.V. All rights reserved.

引用

页码：1 / 7

页数：7

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