缺血预处理对兔心肌细胞凋亡的影响

Effects of ischemic preconditioning on myocyte apoptosis reduced by myocardial ischemia/reperfusion injury (I/R) in rabbits

目的探讨缺血预处理及缺血再灌注对兔缺血再灌注心肌细胞凋亡的影响。方法制备兔缺血预处理(ische-mic preconditioning,IP)、缺血再灌注损伤(I/R)模型,采用末端脱氧核苷酶转换酶介导的生物素平移缺口末端标记技术(trans-ferase-mediated dUTP nick end labeling,TUNEL)检测心肌细胞凋亡情况。结果 RI组细胞凋亡率(43.37±4.82)%,IP组虽然也有一定的心肌细胞凋亡率(24.53±2.95)%,但较I/R组明显降低(P<0.01)。IP组心肌梗死范围较I/R组明显减小。结论心肌缺血再灌注损伤可诱发或加重心肌细胞凋亡,IP能明显减少缺血再灌注诱导的心肌细胞凋亡的发生率,能明显减少心肌梗死范围,减轻缺血再灌注损伤;IP能减少心肌梗死范围、减轻缺血再灌注损伤的机制可能与其能明显减少心肌细胞凋亡有关。

Objective To investigate the effects of ischemie preconditioning(IP)on myocyte apoptosis reduced by myocardial ischemia/reperfusion injury(I/R)in rabbits.Methods An ischcmia reperfusion model of rabbits was developed and used to conduct pre-ischemic transient myocardial isehemic pre-conditioning(IP)).The presence of apoptotic myocytes was demonstrated by the method of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL).Also,the size of myocardial infarct was determined.Results The rate of apoptotic myocytes in IP group was(24.53±2.95)%,higher than that in control group(0.73± 0.51)%,but was signifieantly lower than that in RI groups(43.37±4.82%)(P<0.01).In comparison with those in I/R.infarct sizes in IP groups were significantly reduced(P<0.01).Conclusions IP reduces the extent of myocardial infarction due to myocardial ischemia reperfusion injury in rats.The mechnism of protection could be related to reduced rates of myocyte apoptosis.