肺复张后不同潮气量对急性肺损伤大鼠肺血管内皮舒张功能的影响  

Effects of tidal volume with different amount of gas after recruitment maneuver ventilation on lung vascular endothelial diastole function in rats with acute lung injury

作　　者：王建强[1] 潘纯[2] 刘玲[2] 景亮[3] 杨毅[2] 李国民[1] 袁冬[1] 邱海波[2] 

机构地区：[1]江苏大学附属金坛医院ICU,江苏省金坛213200 [2]东南大学附属中大医院ICU [3]东南大学附属中大医院麻醉科

出　　处：《中华急诊医学杂志》2010年第9期931-937,共7页Chinese Journal of Emergency Medicine

基　　金：江苏省常州市卫生局科研项目（WZ200925）;江苏省金坛市科研项目（TS2007070）

摘　　要：目的 观察肺复张与肺复张后不同潮气量对ALI大鼠肺内皮舒张功能的影响.方法 内毒素（LPS）静脉注射复制大鼠ALI模型.25只清洁级SD大鼠随机（随机数字法）分成5组,每组5只：对照组、ALI组、小潮气量（VT）组（LV组,VT 6 mL/kg）、SI＋小VT组（SI＋LV组,VT 6 mL/kg）、SI＋常规VT组（SI＋MV组,VT12mL/kg）,SI（30 cmH2O）维持30 s,进行肺复张.应用不同潮气量联合肺复张监测呼吸功能和血流动力学,实验5 h后放血处死动物.观察肺组织病理形态改变和湿/干重比（W/D）;放射免疫法检测肺组织中ET-1;免疫组织化学法半定量分析肺动脉内皮细胞内皮型一氧化氮合酶（eNOS）蛋白表达水平;血管张力实验检测离体肺动脉环对乙酰胆碱（Ach）和硝普钠（SNP）介导的舒张功能的影响;ELISA检测肿瘤坏死因子-α（TNF-α）炎症反应指标.结果 与CON组比较,LPS增加各组内肺水肿,加重肺损伤,增加TNF-α含量,增加ET-1含量,减少肺动脉内皮细胞eNOS蛋白表达,减弱Ach介导的内皮依赖的舒张功能,最终影响内皮功能.SI＋LV组ET-1含量为（109.18±15.62）pg/mL,SI＋MV组和LV组肺组织ET-1含量分别为（158.78±30.40）pg/mL和（152.35±8.21）pr/mL,较SI＋LV组升高（P＜0.05）;SI＋LV组肺组织eNOS蛋白表达的iOD值为（12663.83±1348.93）,SI＋MV组和LV组肺组织eNOS蛋白表达的iOD值分别为（9208.12±2773.68）和（9339.53±3366.40）,较SI＋LV组无统计学差异,但有降低趋势（P＞0.05）;与SI＋LV组比较,ALI组和SI＋MV组在不同浓度Ach作用下内皮依赖的舒张功能降低（P＜0.05）,LV组虽然与SI＋LV组比较差异无统计学意义,但Ach介导舒张功能有下降的趋势;SI＋LV组肺组织TNF-α含量（2374.53±410.60）ng/L,较SI＋MV组（3468.86±659.25）ng/L和LV组（3370.75±314.17）ng/L降低（P＜0.05）.结论 肺复张联合大潮气量和小潮气量机械通气能够改善ALI大鼠肺血管内皮舒张功能,肺复张联合Objective To observe the effects of recruitment maneuver （RM） and tidal volume with different amount of gas after RM ventilation on lung diastole function in rats with acute lung injury （ALI）. Method ALI rat models were induced by intravenous infusion of lipopolysaccharide （LPS） in dose of 6 mg/kg. Twenty-five rats were randomly（random number） divided into control group （ n = 5）, ALI group （ n = 5）, low tidal volume group （LV group,VT= 6 mL/kg, n = 5）, sustained inflation （SI） with low tidal volume （SI＋ LV group, VT=6 mL/kg, n = 5）, and SI with moderate tidal volume group （SI＋ MV group, VT= 12 mL/kg, n = 5）. The RM carried out by using SI with airway pressure 30 cmH-2O for 30 seconds, and the positive end-expiratory pressure （PEEP）was set at 5 cmH2O. Lung tissue was taken after mechanical ventilation for 5 hours. The mean arterial pressure （MAP） was monitored throughout the entire course of experiment. Endothelin-1 （ ET-1 ）, endothelial nitricoxide synthase （eNOS）, and acetylcholine-（Ach-） induced endothelium-dependent relaxation response of isolated pulmonary artery rings were investigated after mechanical ventilation for 5 hours. Results The LPS increased the ET-1 level in lung tissue, decreased the level of eNOS in lung tissue, and impaired the Ach-induced endothelium-dependent relaxation response in pulmonary vassals, without obvious influence on systemic hemodynamics. SI ＋ LV significantly reduced LPS-induced elevation of ET-1 level, and increased the level of eNOS, and significantly lessened endothelial dysfunction and ameliorated dysfunction od endothelium-dependent relaxation in pulmonary vas sals. Conclusions RM with high tidal volume or lowtidal volume ventilation could improve the lung vascular endothelial function of rats with acute lung injury, and RM with low tidal volume ventilation could lessen more the injury of lung vascular endothelial diastole function in rats with acute lung injury.

关 键 词：急性肺损伤 肺复张 小潮气量 肺泡内皮细胞 肺动脉舒张 

分 类 号：R563.8[医药卫生—呼吸系统]