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缺氧性肺动脉高压大鼠肺动脉一氧化氮合酶的实验研究
引用本文:崔燕南,马郁文,杜军保.缺氧性肺动脉高压大鼠肺动脉一氧化氮合酶的实验研究[J].北京大学学报(医学版),1999,31(6):0.
作者姓名:崔燕南  马郁文  杜军保
作者单位:北京医科大学第一医院儿科,北京,100034
基金项目:国家自然科学基金,卫生部科研项目 
摘    要:目的:研究大鼠肺动脉中一氧化氮合酶(nitric oxidesynthase,NOS)的含量及分布变化与慢性缺氧性肺动脉高压(hypoxicpulmonary hypertension, HPH)发生的关系。方法:采用eNOS多克隆抗体,对慢性HPH 大鼠的肺组织进行免疫组织化学分析,观察缺氧组及对照组大鼠各级肺动脉中eNOS含量及定位;同时应用分光光度计测定缺氧组及对照组大鼠血浆中NO的间接浓度。结果:正常大鼠肺动脉内皮细胞及平滑肌细胞均含有较高的eNOS表达,且各级肺动脉中eNOS含量差异无显著性;缺氧组大鼠各级肺动脉内皮细胞及平滑肌细胞eNOS含量均较对照组显著减少;缺氧组大鼠血浆NO间接浓度较对照组明显降低。结论:大鼠肺动脉内皮细胞和平滑肌细胞eNOS含量下降及血浆NO浓度下降参与慢性HPH 的形成。

关 键 词:高血压  肺性/流行病学  一氧化氮合酶☆  肺动脉/酶学  一氧化氮/血液

A study on endothelial nitric oxide synthase in pulmonary arteries of hypoxic pulmonary hypertensive rats
CUI Yan-Nan,MA Yu-Wen,DU Jun-Bao.A study on endothelial nitric oxide synthase in pulmonary arteries of hypoxic pulmonary hypertensive rats[J].Journal of Peking University:Health Sciences,1999,31(6):0.
Authors:CUI Yan-Nan  MA Yu-Wen  DU Jun-Bao
Abstract:Objective: To study the abundance and localization of nitric oxide synthase (NOS) in pulmonary arteries of rats and to explore the relationship between their changes and chronic hypoxic pulmonary hypertension (HPH). Methods: Immunohistochemistry technique was performed on the lung tissues of the HPH rats with eNOS multiclonal antibody to assay the abundance and localization of eNOS in different segments of pulmonary arteries of the hypoxic and control rats. At the same time, the plasma concentration of nitric oxide (NO) metabolite, nitrite, was measured by spectrophotometry. Results: eNOS expression was found in pulmonary artery endothelial cells and smooth muscle cells, and there was no significant difference among the different segments of pulmonary arteries, whereas the eNOS expression was inhibited in endothelial cells and smooth muscle cells of pulmonary arteries in hypoxia group; The plasma concentration of nitrite in hypoxia group was significantly decreased compared with that of control rats. Conclusion: The results suggest that the decrease in eNOS in pulmonary artery endothelial cells and smooth muscle cells by hypoxia as well as the decrease in plasma concentration of NO may play a role in the development of chronic HPH.
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