心肌缺血后处理抑制线粒体通透性转换孔开放的研究  

Myocardial Ischemia Postconditioning Inhibits Mitochondrial Permeability Transition

作　　者：康少平[1] 李旭光[1] 董嘉良[1] 张敏[2] 康英姿[1] 张艳君[1] 于公元[1] 

机构地区：[1]天津医科大学生物化学教研室,天津300070 [2]武警医学院生物化学教研室,天津300162

出　　处：《中国实用内科杂志》2008年第S2期40-42,共3页Chinese Journal of Practical Internal Medicine

基　　金：天津市教育委员会科研项目(200011)

摘　　要：目的探讨心肌缺血后处理调节线粒体通透性转换孔开放情况。方法16只Wistar大鼠随机分成2组,对照组(缺血再灌注组)和缺血后处理组,每组8只。采用大鼠离体心脏Langendorf灌流装置,对照组全心缺血30min,再灌注3h;缺血后处理组全心缺血30min后,再灌注30s,缺血30s,反复3次,然后持续再灌注3h。立即取下心肌组织,利用差速离心的方法提取心肌细胞线粒体。分光光度计测定Ca2+诱发的线粒体通透性转换孔(mitochondrial permeability transition pore,mPTP)开放。TTC染色分析心肌梗死面积。结果对照组心肌梗死面积明显高于后处理组(P<0.01)。对照组心肌线粒体细胞色素C(cytochromeC,Cyto C)释放速度和最大释放量均高于后处理组(P<0.01)。结论缺血后处理抑制Ca2+诱导的mPTP开放,减少Cyto C的释放,对缺血再灌注损伤的心肌有保护作用。Objective To explore myocardial ischemia postconditioning whether can inhibit the mitochondrial permeability transition pore(mPTP) opening.Methods Sixteen Wistar rats were randomLy divided into two groups:the control group(ischemia reperfusion group) and the postconditioning group(n=8) .The isolated heart was perfused by the Langendorff method.30 min global myocardial ischemia is given to the rats of control group,and then 3h reperfusion;to the postconditioning group,it consisted of 3 episodes of 30 seconds of coronary occlusion and 30 seconds of reperfusion after the 30 min global myocardial ischemia and then 3h reperfusion.Myocardial mitochondria taken from myocardium were prepared with differential centrifugation.The opening of mPTP was observed by UV spectrophotometer.Infarct size was assessed by triphenyltetrazolium staining.Results The Infarct size of the control group was higher than that of postconditioning group(P<0.01) .The releasing rate and maximum of cytochrome C(Cyto C) of the control group are significantly higher than that of postconditioning group(P<0.01) .Conclusion Postconditioning inhibits opening of the mPTP,decreases the releasing of Cyto C and provides a powerful antiischemic protection.

关 键 词：缺血后处理 再灌注 线粒体通透性转换孔 细胞色素C 

分 类 号：R541[医药卫生—心血管疾病]