热休克、心肌缺血预处理对I/R心肌的第二窗保护作用  

The role of heat shock、ischemic preconditioning in the delayed protection of ischemic preconditioning

作　　者：王悦喜[1] 陈运贞[1] 刘元生[1] 

机构地区：[1]重庆医科大学临床学院心血管内科,重庆400016

出　　处：《重庆医科大学学报》2001年第1期32-33,共2页Journal of Chongqing Medical University

摘　　要：目的：观察IP(ischemic preconditioning，缺血预处理)、HS(heat shock，热休克)对I/R(ischemic/reperfusion，缺血/再灌注)损伤的保护作用。方法：建立Wistar大鼠I/R动物模型，缺血90min后再灌注3h，分为对照组、HS组和 IP组3组，用免疫组化方法检测第二窗保护(second window of protection，SWOP)过程中蛋白激酶C a、d（PKCa、PKCd）的活性，并用TTC染色测定心肌坏死范围。结果：HS组和IP组心肌坏死范围较对照组明显缩小(Ｐ<0.01)，3组PKCa、PKCd均未见从胞浆向细胞膜转位。结论：HS和IP均有心肌保护作用，PKCa、PKCd在SWOP中可能不起作用，其确切机制有待进一步研究。Objective: To observe the protective role of IP and HS on I/Rinjury. Methods:Wistar rats treated with prior whole-body hyperthermia(heat shock) and 24 hours recovery (n =11); or 3 episodes of 5 minutes of IP (ischemic preconditioning) and 24 hours of recovery( n =11);The control rats ( n =11)were sutured under coronary artery but not occluded. After 90 minutes of coronary artery occlusion and 3 hours of reperfusion ,the rats were killed and PKCa and PKCb were tested with immunohistochemical analysis.Results:Infarct size was significantly reduced in HS and IP group compared with control group(Ｐ<0.01).Ventricular samples from all three groups showed no translocation of PKCa and PKCb from cytoplasm to membranes.Conclusion:In this model of I/R (ischemia/reperfusion),prior HS and IP were associated with significantly improved myocardial salvage after 90 minutes and 3 hours reperfusion.The PKCa and PKCb may not play an important role in conferring myocardial protection from I/R injury in this animal model.Further study for the mechanism of SWOP associated with IP was needed.

关 键 词：缺血预处理 心肌保护 热休克 心肌缺血 再灌注损伤 蛋白激酶C SWOP I/R心肌 

分 类 号：R542.2[医药卫生—心血管疾病]