体外膜肺氧合对脂多糖诱导急性肺损伤模型的治疗研究  

The therapeutic study of extracorporeal membrane oxygenation on lipopolysaccharides induced acute lung injury model

作　　者：刘庆亮[1] 张静 李建朝 Liu Qingliang;Zhang Jing;Li Jianzhao(Department of Coronary Care Unit,Henan Provincial People’s Hospital,Zhengzhou 450003,China;Department of Cardiac Intensive Care,Fuwai Central China Cardiovascular Hospital,Zhengzhou 451450,China;Department of Extracorporeal Circulation,Fuwai Central China Cardiovascular Hospital,Zhengzhou 451450,China)

机构地区：[1]河南省人民医院心脏重症科,郑州450003 [2]阜外华中心血管病医院心脏重症科,郑州451450 [3]阜外华中心血管病医院体外循环科,郑州451450

出　　处：《中华实验外科杂志》2023年第11期2270-2273,共4页Chinese Journal of Experimental Surgery

基　　金：河南省医学科技攻关计划项目(LHGJ20220112)。

摘　　要：目的:探讨体外膜肺氧合(ECMO)治疗脂多糖诱导的大鼠急性肺损伤的效果及作用机制。方法:30只健康雄性SD大鼠随机分为对照组、肺损伤组和ECMO组,每组大鼠10只。肺损伤组和ECMO组大鼠麻醉后采用脂多糖静脉注射建立肺损伤模型,ECMO组大鼠在右侧外静脉注射脂多糖后,2 h后开始体外循环,右股动脉转流2 h。对照组和肺损伤组大鼠注射等体积生理盐水。分析3组大鼠干预注射前(T0)、脂多糖或生理盐水注射后4 h(T1)的呼吸频率、动脉血氧分压、肺组织湿重量比值和病理学变化。采用酶联免疫吸附试验(ELISA)试剂盒检测大鼠外周血炎性因子[肿瘤坏死因子-α(TNF-α)和白细胞介素(IL)-1β]的水平;蛋白质免疫印迹分析3组大鼠磷酸化p65和p50表达水平;原位缺口末端标记法(TUNEL)染色分析大鼠肺组织细胞凋亡水平。组间计量数据比较采用单因素方差分析。结果:ECMO组大鼠肺组织呼吸频率[(94.70±2.63)次/分]明显低于肺损伤组[(108.40±7.69)次/分],差异有统计学意义(t=5.330,P<0.05)。ECMO组大鼠血氧分压[(112.10±7.39)mmHg,1 mmHg=0.133 kPa]明显高于肺损伤组[(79.10±4.28)mmHg],差异有统计学意义(t=12.230,P<0.05)。ECMO组大鼠肺组织病理评分[(5.90±1.20)分]明显低于肺损伤组[(10.20±1.33)分],差异有统计学意义(t=27.550,P<0.05)。ECMO组大鼠肺组织湿干比(2.87±0.19)明显低于肺损伤组(3.84±0.17),差异有统计学意义(t=12.220,P<0.05)。ECMO组大鼠外周血炎性因子TNF-α和IL-1β水平[(65.83±12.28)、(60.26±7.60)pg/ml]明显低于肺损伤组[(132.99±14.46)、(89.13±12.83)pg/ml],差异有统计学意义(t=11.190、6.123,P<0.05)。ECMO组大鼠肺组织细胞凋亡水平[(9.99±1.93)%]明显低于肺损伤组[(19.94±3.00)%],差异有统计学意义(t=8.841,P<0.05)。ECMO组大鼠外周肺组织磷酸化p65和p50蛋白表达水平(1.33±0.08、1.27±0.11)明显低于肺损伤组(1.88±0.13、1.74±0.14),差异有统计学意义(t=11.3Objective To investigate the efficacy and mechanism of extracorporeal membrane oxygenation(ECMO)in the treatment of lipopolysaccharide induced acute lung injury in rats.Methods Thirty healthy male SD rats were randomly divided into a control group,a lung injury group,and an ECMO group,with 10 rats in each group.After anesthesia,rats in the lung injury group and ECMO group were injected with lipopolysaccharide intravenously to establish a lung injury model.Rats in the ECMO group were injected with lipopolysaccharide into the right external vein,and extracorporeal circulation began 2 hours later,with a right femoral artery bypass for 2 hours.Rats in the control group and lung injury group were injected with an equal volume of physiological saline.Analyze the respiratory frequency,arterial oxygen partial pressure,lung tissue wet weight ratio,and pathological changes of three groups of rats before intervention injection(T0)and 4 hours after injection of lipopolysaccharide or physiological saline(T1).Peripheral blood inflammatory factors[tumor necrosis factor-α(TNF-α)and interleukin(IL)-1β]in rats were analyzed by enzyme linked immunosorbent assay(ELISA)kit.The level of phosphorylated p65 and p50 expression levels in three groups of rats were of were analyzed by Western blotting.The level of apoptosis in rat lung tissue cells were analyzed by terminal-deoxynucleotidyl transferase mediated nick end labeling(TUNEL)staining.The comparison of inter group econometric data was conducted using one-way analysis of variance.Results The respiratory rate of the lung tissue in the ECMO group[(94.70±2.63)times/min]was significantly lower than that in the lung injury group[(108.40±7.69)times/min,t=5.330,P<0.05].The blood oxygen partial pressure of rats in the ECMO group[(112.10±7.39)mmHg,1 mmHg=0.133 kPa]was significantly higher than that in the lung injury group[(79.10±4.28)mmHg,t=12.230,P<0.05].The pathological score of lung tissue in the ECMO group(5.90±1.20)was significantly lower than that in the lung injury group(10.2

关 键 词：体外膜肺氧合 脂多糖 急性肺损伤 炎症 凋亡 

分 类 号：R563.8[医药卫生—呼吸系统] R-332[医药卫生—内科学]