【摘要】 目的探讨缺血再灌注及缺血预处理对大鼠缺血再灌注心肌细胞凋亡的影响。方法制备大鼠缺血预处理 (IP)、缺血再灌注损伤 (I/R)模型 ,采用末端脱氧核苷酸转换酶介导的生物素平移缺口末端标记技术 (TUNEL)检测心肌细胞凋亡情况 ;同时检测心肌梗死范围。结果I/R组细胞凋亡率 ( 4 3.37±4 .82 % )高 ,IP组虽然也有一定的心肌细胞凋亡率 ( 2 4 .5 3± 2 .95 % ) ,但较I/R组明显降低 (P <0 .0 0 1 )。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理可能与其能明显减少心肌细胞凋亡有关。更多还原

【Abstract】 Objective To investigate the effects of ischemic preconditioning(IP)on myocyte apoptosis reduced by myocardial ischemia/reperfusion injury(I/R) in rats.Methods An ischemia-reperfusion model of rat was established and used to conduct pre-ischemic transient myocardial ischemic pre-conditioning(IP)).The presence of apoptotic myocytes was demonstrated by the method of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL).Also,myocardial infarct size were determined.Results The rate of apoptotic myocytes in IP group (24.53±2.95%)was higher than that in control(0.73±0.51%),but was lower than that in RI groups (43.37±4.82%) significantly(P<0.001).In comparison with those in I/R,infarct sizes in IP groups were significantly reduced(P<0.001).Conclusions IP have a protective effect on injury induced by I/R in rats ,and also reduce the rates of myocyte apoptosis in those situations.The machnism of protective effect could be related to reducing the rates of myocyte apoptosis.更多还原