中文摘要：

目的观察高氧致慢性肺疾病（CLD）新生大鼠肺组织血管紧张素转换酶（ACE）、血管紧张素Ⅱ（AngⅡ）、转化生长因子β1（TGF—β1）的动态变化及卡托普利的保护机制。方法足月新生Wistar大鼠240只，随机分为4组，每组60只。模型组、盐水对照组及卡托普利治疗组将足月新生Wistar大鼠（连同母鼠）置于氧舱内持续吸入高浓度氧（FiO2：0．9）21d造成高氧肺损伤模型，空气对照组吸入空气；卡托普利治疗组于生后7d起经胃管灌服卡托普利30mg·kg^-1·d^-1，盐水对照组每天经胃管灌服等量生理盐水。每组分别于实验开始后的第1，3，7，14，21d随机各选取6只麻醉后处死。采用酶联免疫吸附法测定肺组织TGF-β1的含量，用日产7170全自动生化分析仪测定ACE活性，用放免法测定AngⅡ的含量。采用RT—PCR检测肺组织ACE、AngⅡ、TGF-β1 mRNA表达的动态变化并同时观察肺组织形态学变化。结果4组肺组织ACE、AngⅡ和TGF—β1的含量及mRNA表达在实验后1，3，7d差异无统计学意义（P〉0．05）；模型组、盐水对照组14d明显升高，21d达高峰，与空气对照组比较差异显著（P〈0．05或0．01）；卡托普利治疗组14和21d与模型组、盐水对照组比较明显降低（P〈0．05或0．01），但仍高于空气对照组（P〈0．05）。模型组、盐水对照组实验后1d肺组织形态学同空气对照组，14d出现肺组织纤维化改变，21d出现严重纤维化。卡托普利治疗组肺组织纤维化病变明显减轻。结论高氧致CLD新生大鼠肺组织ACE、AngⅡ、TGF-β1含量及mRNA表达在高氧后14和21d明显增高，同时肺组织出现纤维化改变，应用卡托普利干预后上述指标明显低于模型组及盐水对照组．肺纤维化病变明显减轻，表明卡托普利对高氧肺损伤具有一定的保护作用。

英文摘要：

Objective To observe the dynamic changes and the effects of rennin-angiotensin system,TGF-β1 and Captopril on interstitial fi- brosis in lung tissues of neonatal rats with CLD induced by hypemxia. Methods 240 term neonatal Wistar rots were randomly divided into 4 groups （ n = 60 each）. The air control group was exposed to air （ FiO2=0.21 ）. The other three groups were continuously exposed to hyperoxia （ FiO2=0.9. During the exposure,the Captopril treated group received Captopril （30 mg·kg^-1·d^-1） by intmgastric administration, while the normal saline control group was adnfinistrated with normal saline instead. The model group received no treatment. On the 1st,3rd, 7th ,14th day and 21st days of exposure,the subjects were sacrificed. The changes of ACE,Ang Ⅱ ,TGF-β1 and mRNA expression were measured by enzyme-linked immunosorbentassay,mdio-immunity technique and RT-PCR. The changes of lung histomorphology were observed. Results The ACE,Ang-Ⅱ ,TGF-β1 levels and mRNA expression increased significantly in the model and nomual saline control groups on the 14th and 21st days of exposure compared with those of the air control group （P 〈 0.05 ,or P 〈 0.01 ）. Captopril treatment reduced significantly the level and mRNA expression of ACE,Ang Ⅱ ,TGF-β1 and there was no significant difference on the 1st,3rd and 7th days between the model and normal saline control groups and the air control group （P 〉 0.05 ）. But there were significant differences in the level and mRNA expression of ACE,Ang Ⅱ and TGF-β1 between the Captopril-treated group and the air control group. The histopathological examination demonstrated fibrosis in the Model group and Normal saline control group compared with control group. Conclusion The changes in levels and mRNA expression of ACE,Ang Ⅱ and TGF-β1 may be increased significantly on the 14 th and 21st days in lung tissues of neonatal rats with CLD induced by hyperoxia. The histopathological examination can demonstrate fibrosis in the CLD induced by hypero