Effects of exogenous hydrogen sulfide on inflammatory responses during acute myocardial ischemia in rats
10.3760/cma.j.issn.0254-1416.2014.02.028
- VernacularTitle:外源性硫化氢对大鼠急性心肌缺血损伤时炎性反应的影响
- Author:
Fang LIU
;
Guangjie LIU
;
Jianxin ZHANG
;
Lanfang LI
- Publication Type:Journal Article
- Keywords:
Hydrogen sulfide;
Myocardial ischemia;
Inflammation
- From:
Chinese Journal of Anesthesiology
2014;34(2):227-229
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effects of exogenous hydrogen sulfide on inflammatory responses during acute myocardial ischemia in rats.Methods Twenty-four adult male Sprague-Dawley rats,weighing 250-290 g,were randomly divided into 3 groups (n =8 each):sham operation group,acute myocardial ischemia group,and sodium hydrosulfide (NaHS) group.The animals were anesthetized with intraperitoneal chloral hydrate.The model of acute myocardial ischemia was established by ligating the left anterior descending branch of coronary artery.Normal saline 2 ml/kg and NaHS 3.12 mg/kg were intraperitoneally injected at 3 h of ischemia in AMI and NaHS groups,respectively.The rats were sacrificed at 6 h after ligation and hearts were removed for determination of interleukin-1β (IL-1β),IL-6 and tumor necrosis factor-α (TNF-α) contents (by ELISA) and intercellular adhesion molecule-1 (ICAM-1) mRNA expression (by semi-quantitative PCR) in myocardial tissues and for examination of myocardial ultrastructure with transmission electron microscope.Results Compared with S group,IL-1β,IL-6 and TNF-α conte.nts and ICAM-1 mRNA expression in myocardial tissues were significantly increased in AMI group (P ＜ 0.05).Compared with AMI group,IL-1β,IL-6 and TNF-α contents and ICAM-1 mRNA expression in myocardial tissues were significantly decreased in NaHS group (P ＜ 0.05).The damage to myocardial ultrastructure was significantly alleviated in NaHS group when compared with AMI group.Conclusion The mechanism by which exogenous H2S alleviates the acute myocardial ischemia injury is related to inhibition of the inflammatory responses in rats.
