摘要
目的观察大鼠急性心肌缺血早期肺组织细胞凋亡情况,进一步证实此过程中肺损伤的程度。方法健康成年雄性SD大鼠24只,随机均分为两组,假手术组(S组),急性心肌缺血模型(C组)。取肺组织切片行TUNEL染色,计算CAO3、6h细胞凋亡率(RA);肺组织蛋白中caspase-3活性变化。结果 C组肺组织RA明显高于S组(P<0.05)。两组CAO6h时RA值和caspase-3活性明显高于CAO3h时(P<0.05)。肺组织蛋白中caspase-3活性C组高于S组,但差异无统计学意义。结论急性心肌缺血后大鼠肺组织细胞可能通过caspase-3激活途径凋亡数增加,并随时间延长而增加。
Objective To evaluate the apoptosis of lung tissue during acute myocardial isehemia, and further to confirm the degree of injury. Methods Twenty-four adult male rats were equally randomized into 2 groups： group S （sham operation） and group C. The left anterior descending branch of coronary artery was ligated in group C. The lung tissue was sectioned for TUNEL straining at 3 h or 6 h after ischemia. Then CAO 3 h, numbers of apoptosis cells and RA were calculated, and caspase-3 activity was estimated. Results The apoptotic rates of the lung cells and activity of caspase-3 were significantly higher in group C than those in group S （P〈0.05）. At 6 hr, the RA value and caspase-3 activity was obviously higher than that at 3hr in both groups. Conclusion Rat of lung tissue increased after acute myocardial ischemia by caspase-3 activation pathways increase in the number of apoptotic and increase with time.
出处
《临床麻醉学杂志》
CAS
CSCD
北大核心
2012年第10期1017-1018,共2页
Journal of Clinical Anesthesiology
关键词
急性心肌缺血
肺组织细胞
凋亡
Acute myocardial isehemia
I.ung tissue cell
Apoptosis
