热休克、心肌缺血预处理对I/R心肌的第二窗保护作用

王悦喜; 陈运贞; 刘元生

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热休克、心肌缺血预处理对I/R心肌的第二窗保护作用

更新时间：2024-01-17

- 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
- 重庆医科大学学报 2001年第1期页码：32-33
- 作者机构：
  
  重庆医科大学临床学院心血管内科,重庆,400016
- 作者简介：
- 基金信息：
- DOI：
  中图分类号： R542.22
- 纸质出版日期：2001，
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[1]王悦喜,陈运贞,刘元生.热休克、心肌缺血预处理对I/R心肌的第二窗保护作用[J].重庆医科大学学报,2001(01):32-33.

The role of heat shock、ischemic preconditioning in the delayed protection of ischemic preconditioning[J]. Journal of Chongqing Medical University, 2001,(1):32-33.
[1]王悦喜,陈运贞,刘元生.热休克、心肌缺血预处理对I/R心肌的第二窗保护作用[J].重庆医科大学学报,2001(01):32-33. DOI：

The role of heat shock、ischemic preconditioning in the delayed protection of ischemic preconditioning[J]. Journal of Chongqing Medical University, 2001,(1):32-33. DOI：

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。

Abstract

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

预处理心肌保护心肌缺血再灌注损伤蛋白激酶C

Keywords

preconditioningmyocardial protectionIschemia/reperfusion injuryProtein kinase C

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