细胞凋亡在兔体外循环肺损伤中的作用  

Effect of apoptosis on lung injury following cardiopulmonary bypass

作　　者：高铭鑫[1] 张帆[1] 李海涛[1] 白辰[1] 于洋[1] 

机构地区：[1]北京市心肺血管疾病研究所首都医科大学附属北京安贞医院心外科六病房,100029

出　　处：《中华实验外科杂志》2013年第12期2631-2633,F0003,F0004,共5页Chinese Journal of Experimental Surgery

基　　金：国家自然科学基金资助项目（81070204）

摘　　要：目的 探讨细胞凋亡在体外循环（CPB）肺损伤中的作用机制.方法 选取健康新西兰大白兔20只,随机分为CPB组和对照组（Sham组,单纯开胸）.测定各组围CPB期左右心房中性粒细胞计数、氧合指数;取肺组织样本,电镜观察其超微结构,并动态记录肺组织含水量、细胞凋亡相关因子B淋巴细胞/白血病-2（bcl-2）、bcl-2相关X蛋白（bax）、Fas配体（FasL）的表达和bcl-2/bax及细胞凋亡指数变化.结果 CPB后,CPB组较Sham组氧合指数明显下降（P＜0.05）,中性粒细胞在肺内明显聚集（P＜0.05）,肺组织含水量显著增加（P＜0.05）.同时,肺组织细胞凋亡指数明显升高[CPB 30 min,（51.13 ±9.87）‰比（1.27-1.03）‰,P＜0.05;CPB停止即刻,（59.64±7.74）‰比（1.30±0.82）‰,P＜0.05],肺泡上皮细胞FasL蛋白表达增加[CPB 30 min,（53.84±8.64）％比（4.25±1.41）％,P ＜0.05;CPB停止即刻,（81.88±9.67）％比（4.32±1.32）％,P＜0.05],bax蛋白表达增加[CPB 30 min,（56.78±9.12）％比（6.69±1.00）％,P＜0.05;CPB停止即刻,（77.28±8.48）％比（6.96±1.03）％,P＜0.05],bcl-2蛋白表达下降[CPB 30 min,（15.25±1.98）％比（22.87±3.15）％,P ＜0.05;CPB停止即刻,（10.35±1.67）％比（23.54±2.34）％,P＜0.05].结论 体外循环可引发炎性肺损伤,并通过外源性及内源性凋亡途径诱发肺组织细胞凋亡.Objective To study the effect of apoptosis on lung injury after cardiopulmonary bypass （CPB）.Methods Twenty New Zealand rabbits were selected and randomly divided into two groups：CPB group undergoing CPB; Sham group only receiving open chest operation.Blood neutrophils count from right and left atrium and oxygenation index in the two groups were determined perioperatively.Lung water content,bcl-2 protein,bax protein,Fas ligand （FasL） protein,bcl-2/bax,apoptosis index and pathomorphological changes were measured in the lung tissues.Results After CPB,as compared with Sham group,the lung water content （P ＜ 0.05）,neutrophils count （P ＜ 0.05） and oxygenation index （P ＜ 0.05） were significantly elevated in CPB group.Moreover,CPB could increase the expression of FasL （CPB 30 min,53.84±8.64 vs.4.25 ± 1.41,P＜0.05; CPB termination,81.88 ±9.67 vs.4.32 ± 1.32,P＜0.05） and bax （CPB 30 min,56.78 ±9.12 vs.6.69 ± 1.00,P＜0.05; CPB termination,77.28 ±8.48 vs.6.96 ± 1.03,P ＜ 0.05） on alveolar epithelial cells and decrease the expression of bcl-2 （CPB 30 min,15.25 ± 1.98 vs.22.87 ± 3.15,P ＜ 0.05 ; CPB termination,10.35 ± 1.67 vs.23.54 ± 2.34,P ＜ 0.05） and could also promote pathomorphological changes in the lung tissue.Conclusion CPB can induce inflammation of lung tissue and apoptosis through the endogenous and exogeneous apoptosis pathways.

关 键 词：体外循环 肺损伤 脱噬作用 

分 类 号：R654.1[医药卫生—外科学]