缺血后处理对抗大鼠离体心脏缺血再灌注损伤及其作用机制  

Cardioprotection of ischemic postconditioning against ischemia/reperfusion injury in isolated rat hearts

作　　者：吕萍萍[1] 朱立[1] 郦阳明[1] 陈莹莹[1] 沈岳良[1] 

机构地区：[1]浙江大学医学院生理学教研室,浙江杭州310058

出　　处：《中国病理生理杂志》2008年第5期849-851,共3页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30470635);浙江省教育厅科研基金资助项目(No.20061414)

摘　　要：目的:研究缺血后处理(postconditioning)对抗大鼠离体心脏缺血再灌注损伤及其作用机制。方法:采用SD大鼠心肌缺血/再灌注模型,并于再灌注一开始即给予3次全心停灌30s,再灌30s处理作为缺血后预处理。记录心肌收缩功能指标,以Evensblue-TTC法监测心肌梗死范围,并对心律失常严重程度进行定量分析。结果:缺血后处理组左室峰压(LVSP)、最大左室收缩速率(+dp/dtmax)以及心率明显高于缺血对照组。缺血后处理可明显缩小心肌梗死范围(22.97%±3.96%vs缺血对照组44.30%±13.61%,P<0.01)。观察复灌10min时心律失常评分发现,缺血后处理组明显低于缺血对照组。缺血后处理组和缺血预处理组具有类似的心肌保护作用。5-HD组LVSP和+dp/dtmax低于缺血后处理组,心律失常评分增高,心肌梗死范围扩大。结论:缺血后处理对大鼠缺血再灌注损伤具有心脏保护作用,其作用机制可能是部分通过激活线粒体ATP依赖性钾离子(mitoKATP)通道起作用。AIM： To investigate the protective role of postconditioning in myocardial ischemia/reperfusion in rats and its mechanisms. METHODS ： Cardiac contractility was analyzed by the Langendorff method. Infarct size was determined by dual staining with triphenyltetrazolium chloride and Even＇s blue dye, and the cardiac arrhythmia was evaluated. postconditioning was conducted by 3 cycles of 30 s iscbemia followed by 30 s of reperfusion at the beginning of subsequent persistent reperfusion. RESULTS： Left ventricular systolic pressure （LVSP） and maximal rise rate of ventricular pressure （＋dp/dtmax） were higher during reperfusion in postconditioning group compared with control, postconditioning reduced the infarct size in ischemia/reperfusion rat hearts. The cardiac arrhythmia score was decreased in postconditioning group in the first 10 min of reperfusion followed by ischemia compared to control group, postconditioning had similar cardioprotective effect as preconditioning. 5-HD, a selective mitochondrial ATP- sensitive potassium channel （mitoKATP） inhibitor, blocked the amelioration of contract function provided by postconditioning. It also abolished the protective effect of postcon- ditioning on cardiac arrhythmia score and infarct size. CONCLUSION： The results show that postconditioning has cardio-protective effect and attenuates reperfusion injury in ischemic heart. The effect might be partly through the activation of mi-toKATP channel.

关 键 词：缺血预处理 再灌注损伤 钾通道 心脏 

分 类 号：Q463[生物学—生理学]