mitoK(ATP)介导硫化氢预处理延迟相的心肌保护效应  

mitoK(ATP)Mediates the Protective Effect of Late Phase of Hydrogen Sulfide Preconditioning on Myocardial Cells

作　　者：李双凤[1,2] 王亚平[1] 冉珂[1] 唐正国 王丹[1] 肖艳英[1] 

机构地区：[1]中南大学湘雅二医院麻醉科,410011 [2]海南省人民医院麻醉科 [3]长沙市第三医院麻醉科

出　　处：《天津医药》2011年第7期638-640,共3页Tianjin Medical Journal

基　　金：湖南省卫生厅资助项目(项目编号:B2009110)

摘　　要：目的:研究线粒体ATP敏感性钾通道[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-羟葵酸(5-HD)+硫化氢预处理组(HD组),每组8只。Sham组仅穿线但不阻断左冠状动脉前降支(LAD);IR组结扎LAD30min,松解后再灌注120min;HS组静脉注射硫化氢供体NaHS50μg/kg,24h后同IR组处理;HD组于结扎前15min静脉注射5-HD5mg/kg,其他同HS组处理。检测心室面积、心肌缺血面积和梗死面积,计算缺血和梗死面积百分比;电镜下观察心肌细胞超微结构。结果:3组缺血面积百分比差别无统计学意义(P>0.05);HS组心肌梗死面积百分比低于IR组和HD组(P<0.01或P<0.05),HD组与IR组相比差异无统计学意义(P>0.05)。心肌细胞超微结构损伤程度HS组较IR组明显减轻,而HD组与IR组差异不大。结论:硫化氢预处理延迟相可保护缺血再灌注损伤的心肌,mitoK(ATP)介导了硫化氢预处理延迟相的心肌保护通路。Objective：To investigate the protective effect of hydrogen sulfide induced late phase preconditioning on rat myocardial cells with mitochondrial ATP sensitive potassium channel [mitoK（ATP）] activation.Methods：Thirty-two adult male SD rats were randomly divided into 4 groups including Sham group,ischemia and reperfusion（IR） group,hydrogen sulfide treatment（HS） group and 5-hydroxy decanoate（5HD） ＋ HD group（n= 8 for each group）.In Sham group,rats were threaded left anterior descending（LAD） coronary artery,but no blockage.In IR group,rats were tied LAD for 30 min,then reperfusion for 2 h.In HS group,rats were injected donor of hydrogen sulfide-sodium hydrosulfide 50 μg/kg via vein,after 24 h with the same treatment with IR group.In HD group,rats were injected 5-HD（5 mg/kg） 15 min before ligated LAD via vein,then with same treatment with other HS group.The ventricular area,myocardial ischemia and infarct area were determined,and the percentages of ischemic area and infarct area were calculated.The myocardial ultrastructure was observed by electron microscope.Results：There were no significant differences in the percentage of ischemic area between three groups（P 〉 0.05）.Compared with IR group and HD group,the percentage of infarct area was reduced in HS group（P 〈 0.01 or P 〈 0.05）,but no significant difference was found between HD group and IR group（P 〉 0.05）.The damage of myocardial ultrastructure was less severe in HS group than that of IR group,but no significant difference between IR group and HD group.Conclusion：Hydrogen sulfide delayed preconditioning can protect the cardiomyocytes by activating the mitoK（ATP） channel.

关 键 词：KATP通道 线粒体质子转运ATP酶 缺血预处理 心肌 心肌再灌注损伤 硫化氢 心肌梗死 心肌缺血 大鼠 SPRAGUE-DAWLEY 

分 类 号：R654.2[医药卫生—外科学]