天津医药

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mitoK(ATP)介导硫化氢预处理延迟相的心肌保护效应

李双凤   

  1. 海南省人民医院麻醉科
  • 收稿日期:2010-07-28 修回日期:2011-04-18 出版日期:2011-07-15 发布日期:2011-07-15
  • 通讯作者: 李双凤

mitoK(ATP) mediates the protective effect of hydrogen sulfide delayed preconditioning on myocardial cells

  • Received:2010-07-28 Revised:2011-04-18 Published:2011-07-15 Online:2011-07-15

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摘要： 摘要 目的：研究mitoK(ATP)激活在硫化氢预处理延迟相对大鼠心肌细胞的保护效应。方法：将32只健康成年雄性SD大鼠随机分成假手术组（Sham组）、缺血再灌注组（IR组）、硫化氢预处理组（HS组）和5-HD+硫化氢预处理组（HD组），每组8只。Sham组仅分离左冠前降支，不阻断血流150 min，IR组阻断左冠前降支30 min，再灌注120 min，HS组静脉注射硫化氢供体NaHS 50μg/kg，24h后同IR组处理，HD组阻断前15min静脉注射5-HD(5-hydroxydecanoate ) 5mg/Kg，其它同HS组处理。检测心肌缺血面积和梗死面积；电镜下观察心肌细胞超微结构。结果：HS组心肌梗死面积百分比和心肌细胞超微结构损伤低于IR组和HD组(P<0.05)，HD组与IR组相比差异无统计学意义(P>0.05)；结论：硫化氢预处理延迟相可保护缺血再灌注损伤的心肌，线粒体ATP敏感性钾通道[mitoK(ATP)]介导了硫化氢预处理延迟相的心肌保护通路。

关键词: 硫化氢, 预处理, 缺血再灌注, 钾通道

Abstract: Abstract: Objective To investigate the protective effect of hydrogen sulfide delayed preconditioning with mitochondrial ATP sensitive potassium channel[mitoK(ATP)] activation on rat myocardial cells. Methods Thirty-two S-D adult male rats were randomly divided into a Sham group, an IR group, a HS group and a HD group(n = 8). In Sham group, we isolated left anterior descending(LAD) coronary artery, but not blocked for 150 minutes; in IR group, we blocked LAD for 30 min and then primed for 2h; in HS group, we injected donor of hydrogen sulfide — sodium hydrosulfide 50μg/kg via vein, after 24h, dealed the same with IR group; in HD group, we injected 5-HD 15min before blocking LAD via vein, others dealed the same with HS group. the myocardial infarct size and area at risk were determined; the myocardial ultrastructure was observed by electron microscope. Results Compared with IR group, the infarct size was reduced and the damage of myocardial ultrastructure was depressed in HS group(P<0.05). Compared with IR group, there was no significant difference in HA group(P>0.05). Conclusion Hydrogen sulfide delayed preconditioning can protect the cardiomyocytes by activating the KATP channel.

Key words: hydrogen sulfide, preconditioning, ischemia reperfusion, potassium channel