野百合碱致大鼠肺动脉高压时SOD活性和MDA含量的变化

Changes in activity of superoxide dismutase and content of malondi-aldehyde in rats with monocrotaline-induced pulmonary hypertension

目的:观察超氧化物岐化酶(SOD)活性和脂质过氧化反应产物丙二醛(MDA)含量在野百合碱(MCT)引起大鼠肺动脉高压(PH)模型时的变化.方法:给SD大鼠背部皮下一次注射MCT(60mg/kg)复制PH模型,用比色分析法测定静脉血浆和肺匀浆中SOD活性和MDA含量,用彩色图像分析仪观察测定直径小于100μm的肺小动脉中膜厚度.结果:在注射MCT4周后,血浆中SOD活性对照组为(159±28)NU(硝酸盐单位)/ml,MCT组为(106±45)NU/ml(PM<O.05);肺匀浆中SOD活性两组分别为(505±47)和(317±59)NU/ml(P<0.01).血浆和肺匀浆中MDA含量MCT组为(15±5)和(59±14)μmol/L,对照组为(5.3±2.8)和(32±19)μmol/L(P<0.05和P<0.01).MCT组肺小动脉中膜明显增厚.结论:MCT可损伤肺血管内皮,导致肺脏清除O_2的能力下阵,脂质过氧化增强和NO生成减少,这可能是MCT形成PH的重要原因.

Objective: To observe the changes in activity of superoxide dismutase (SOD) and content of mal-ondialdehyde (MDA) in pulmonary hypertension (PH). Methods: Adults male Sprague-Dawley rats were given a single subcutaneous injection of monocrotaline (MCT, 60 mg/kg) to induced the mold of PH. Activity of SOD and contents of MDA in plasma and pulmonary homogenate were measured by colorimetric analysis. Medial thickness of pulmonary small arteries (external diameter<100μm) were measured using colour image analysis system. Results: Four weeks after injection of MCT, activity of SOD in venous plasma was (106±45) NU/ml (P<0. 05) and (317±59) NU/ml (P<0. 01) in pulmonary homogenate for MCT group, while (159±28) NU/ml (P<0. 05), (505±47) NU/ml (P<0. 01) respectively for the controls. Contents of MDA were (15±5), (59±14)μmol/L for MCT group, while (5. 3±2. 8), (32±19) μmol/L for the controls; Medial thickness of pulmonary small arteries increased significantly. Conclusion: The main cause of PH development is the injury of pulmonary endothelial cells by MCT, which decreases the ability of removing O2., enhances lipid peroxidation, reduced NO production, so as to induce PH.