摘要
目的 探讨微量去甲肾上腺素预处理对大鼠缺血再灌注心肌细胞凋亡的影响并与缺血预处理比较。方法 采用大鼠在体缺血再灌注 (I/R)模型 ,分别以缺血前去甲肾上腺素预处理 (NE -P) ,缺血预处理 (IP) ,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)检测各组心肌细胞凋亡情况 ;同时检测心肌梗死范围。结果 I/R组细胞凋亡率〔(4 3 33± 4 92 ) %〕较高 ,NE -P组及IP组虽然也有一定的心肌细胞凋亡率〔(2 5 2 4± 1 5 6 ) %、(2 4 44± 2 96 ) %〕 ,但较I/R组明显降低 (P <0 0 0 1)。IP组及NE -P组心肌梗死范围较I/R组明显减少 ,IP组及NE -P组两项指标无显著差异。结论 心肌缺血再灌注损伤可诱发心肌细胞凋亡 ,NE -P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 ;NE -P减少心肌梗死范围。
Objective To investigate the effects of NE pretreatment(NE-P) and ischemic preconditioning(IP) on myocyte apoptosis reduced by myocardial ischemia reperfusion injure(I/R) in rats.Methods Aischemic-reperfusion model of rat was used to conduct NE pretreatment and ischemic preconditioning.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 NE-P group 〔(25 24±1 56)%〕 and IP group 〔(24 44±2 96)%〕 was higher than that in control 〔(0 71±0 51)%〕, but was lower than that in I/R groups 〔(43 33±4 92)%〕 significantly( P <0 001). In comparison with those in I/R ,infarct sizes in NE-P group and IP groups were significantly reduced ( P <0 01) Conclusions NE-P have a protective effect on injure 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. [
出处
《中国急救医学》
CAS
CSCD
北大核心
2001年第8期442-444,共3页
Chinese Journal of Critical Care Medicine
基金
20 0 0年湖北省教育厅科研基金资助 (项目编号 2 0 0 0B440 0 9)