中文摘要：

目的研究大鼠急性肺损伤时循环及肺组织血管紧张素Ⅱ（AngⅡ）含量的变化，探讨AngⅡ在急性肺损伤发病中的作用。方法清洁级SD大鼠30只，随机分为正常对照组（n=6）和模型组（n=24），模型组又按注射脂多糖（12S）后3、6、9、12h四个时间点分成4组，每组6只。分别于静脉注射IPS后各分组时间点观察大鼠一般情况、血压、动脉血气分析、肺组织湿质量／干质量（W／D）比值、肺组织病理改变，放免法测定血浆及肺组织AngⅡ的含量的变化，所有观察指标采用单因素方差分析与正常对照组比较。结果与正常对照组比较，pH值和动脉血氧分压显著降低（P〈0．05），而二氧化碳分压及肺W／D比值均显著高于对照组（P〈0．05），病理形态学积分分析显示肺组织受损（P〈0．01）。ALI大鼠血浆及肺组织AngⅡ均升高（P〈0．05），其中血浆AngⅡ在9h时点达峰值，而组织AngⅡ浓度在各观察时间点持续上升。结论ALI时肺组织和血中AngⅡ大量释放，提示ALI时伴有全身及肺局部肾索一血管紧张素系统的激活。

英文摘要：

Objective To investigate the changes in circulatory and pulmonary monary angiotensin Ⅱ in rats with acite lung injury （ALI） and explore the role of angiotensin Ⅱ in ALI. Method Thirty S-D rats were randomly divided into control group （ n = 6） and ALI group （ n = 24）. The ALI group was further divided into four subgroups of observation at various intervals, 3, 6, 9 and 12 hours after administration of lipopolysaccharide （LPS） into the femoral vein （each n = 6）. The indices rate, blood gas analysis, wet weight/dry weight （W/D） ratio of lung lobes, and pathological changes were successively observed at 3, 6, 9, and 12 hours after injury. The content of angiotensin Ⅱ in lung tissue and blood plasnm were detected at above set intervals by radioimmunoassay. Data of these assays were analyzed by one-factor analysis of vmiance. Results Compare with the control group, pH and PaO2 of arterial blood in ALI group decreased significantly （ P 〈 0.05） at all intervals and PaCO2 of arterial blood in ALI group decreased significantly （P 〈 0.05）. at all intervals and PaCO2 of arterial blood and lung W/D weight ratio increased significantly （P 〈 0.05）, and scores of lung histopathology denoted the lung injuried （P 〈 0. 01）. After injury of lung, angiotensin Ⅱ content increased markedly in lung homogenate and blood plasma （ P 〈 0.05）. Angiotensin Ⅱ content in blood plasma reached peak value at 9 hours, and content of angiotensin Ⅱ in lung homogenates kept on increasing at allintervals of observation. Conduslons A large amount of angiotensin Ⅱ releases into lung tissue and blood plasma during ALI, suggesting systemic and pulmonary rennin-angiotensin systems are activated.