摘要
目的：观察低氧高二氧化碳对肺组织超氧化物岐化酶(SOD)、过氧化氢酶(CAT)活力及丙二醛(MDA)含量的影响,探讨氧化应激于低氧高二氧化碳肺动脉高压形成发展中的作用。方法：复制低氧高二氧化碳肺动脉高压大鼠模型。测定平均肺动脉压(mPAP)、右心室／(左心室+室间隔)[RV／(LV+S)]比。比色法测定肺组织SOD、CAT活力及MDA含量。电镜观察肺血管组织细胞超微结构。结果：与对照组相比,各低氧高二氧化碳组mPAP、RV／(LV+S)比明显升高(均P＜0.01),肺组织SOD、CAT活力均显著降低,而MDA含量明显升高(分别P＜0.05,P＜0.01)。电镜下,低氧高二氧化碳肺动脉高压大鼠肺中小肌型动脉内皮细胞及平滑肌细胞增殖、肥厚、肿胀,胶原纤维亦增生插入平滑肌细胞。结论：低氧高二氧化碳时大鼠肺组织氧化应激参与肺动脉高压的形成与发展。
Objective：To study the effect of hypoxia and hypercapnia on superoxide dismutase （SOD）,catalase （CAT）,malondialdehyde （MDA） in rat lung tissue,and explore the effect of oxidative stress on the developument of the pulmonary hypertension. Methods： The model of hypoxic and hypercapnic pulmonary hypertension was made. Mean pulmonary pressure （mPAP） and the ratio of right ventricule to left ventricule and septum [RV/（LV＋S）] were tested. The contents of CAT and SOD and MDA in rat lung were determined by spectophotumetry. The ultrastrutural changes in rat lung were observed. Results： The values of mPAP and RV/（LV＋S） showed significantly higher in all hypoxic and hypercapnic group compared with control group （all of P〈 0.05, respectively）. The activities of SOD and CAT in lung homogenates were significantly lowered, but MDA significantly higher in hypoxic and hypercapnic group compared with control group （P〈 0.05, P〈 0.01, respectively）. Ultrastructural changes, such as hyperplasia, hypertrophy and swelling of endothelial and smooth muscle cells, and hypertrophic collogen intervening into smooth muscle cell were found under electron microscope in medium and small intrapulmonary muscularized arteries of hypoxic and hypercapnic pulmonary rat lung. Conclusion： Oxidative stress in rat lung caused by hypoxia and hypercapnia plays an important role in the development of pulmonary hypertension.
出处
《温州医学院学报》
CAS
2005年第6期437-439,共3页
Journal of Wenzhou Medical College
基金
浙江省自然科学基金(No.396479)
关键词
低氧
高碳酸血症
肺动脉高压
氧自由基
氧化应激
hypoxia
hypercapnia
pulmonary hypertension
oxygen radicals
oxidative stress
