大鼠肺缺血再灌注损伤引起肺细胞的凋亡

目的:观察肺缺血再灌注损伤对肺细胞凋亡的影响.方法:雄性SD大鼠40只,体质量300～350 g,随机分为8组(缺血再灌注6组,单纯缺血组,对照组),每组5只.通过阻断肺门建立大鼠原位肺缺血再灌注模型,应用末端脱氧核苷酸转移酶(TdT)介导的dUTP缺口末端标记技术(TUNEL)检测缺血再灌注损伤所引起的肺细胞凋亡的变化及其与再灌注时间的相关性;DNA电泳进行肺组织细胞DNA片段分析;电镜观察凋亡细胞的超微结构.结果:在肺缺血再灌注后早期(30 min)发生明显的肺细胞凋亡,凋亡细胞数峰值位于再灌注后2 h,再灌注后12 h凋亡细胞数与对照组无显著差别;缺血而无再灌注的肺细胞凋亡无明显变化.结论:细胞凋亡在肺缺血再灌注损伤机制中可能起着重要作用.

Pulmonary apoptosis induced by ischemia-reperfusion lung injury in rats

Objective:To observe the pulmonary apoptosis resulted from ischemia reperfusion lung injury in rats. Methods: Forty male SD rats, weighing 300 350 g,were randomly divided into 8 groups: 6 ischemia reperfusion group,simple ischemia group and control group( n =5).An in situ ischemia reperfusion lung injury rat model was established. Apoptotic cells were detected by the terminal deoxynucleotidyl transferase mediate dUTP nick end labelling (TUNEL) technique and the apoptotic DNA fragments by pulmonary DNA electrophoresis. Electron microscopy was performed to verify the morphologic changes of apoptosis. Results: Obvious apoptosis of pneumocytes occurred early after(30 min) ischemia reperfusion lung injury, with the peak on 2 h after reperfusion, and there were no significant differences 12 h after reperfusion compared with control group. There was a slight but no statistically significant elevation of apoptotic pneumocytes number in simple ischemia group compared with controls. Conclusion: The result indicates that apoptosis may contribute significantly to ischemia reperfusion lung injury.