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目的 研究内源性一氧化碳 /血红素氧合酶 (CO/HO)体系在慢性低氧环境中的变化规律 ,探讨CO/HO体系在缺氧性肺动脉高压形成中的作用。方法 将第 1批大鼠随机分为对照组、低氧 1d组、低氧 3d组、低氧 7d组、低氧 14d组 ;第 2批大鼠随机分为对照组、低氧组、低氧 +锌原卟啉(ZnPP)组。均以右心导管法测定肺动脉压力 ;称量并计算右心室与左心室加室间隔的比例 ;应用双波长分光光度计法间接测定大鼠血浆及肺组织匀浆中CO含量 ;应用免疫组织化学技术对第一批大鼠肺内HO 1蛋白表达进行定位及半定量分析。结果 大鼠低氧 7～ 14d开始形成稳定的肺动脉高压 ,伴右心室肥大 ;血浆及肺组织匀浆中CO含量分别于低氧 1d和低氧 14d时两次明显增高 (P <0 0 1) ;低氧 1～ 3d肺泡及肺泡间质巨噬细胞和炎性细胞HO 1表达增多 ,低氧 7～ 14d后肺泡水平肺动脉中膜平滑肌细胞HO 1表达显著增高 (F =8 72 ,P <0 0 0 1)。低氧 +ZnPP组大鼠肺动脉平均压明显高于对照组及低氧组 ,血浆及肺组织匀浆中CO含量明显低于低氧组 (P均 <0 0 1)。结论 内源性CO/HO体系在慢性低氧刺激下明显增高 ,且呈时间依赖性的双峰现象 ,其中第 2次代偿性增高与肺动脉压力的变化密切相关 ,HO 1抑制剂的干预研究进一步表明 ,内源性CO/HO体系对缺
Objective To investigate the changes of endogenous carbon monoxide / heme oxygenase (CO / HO) system in chronic hypoxic environment and to explore the role of CO / HO system in hypoxic pulmonary hypertension. Methods The first rats were randomly divided into control group, hypoxia 1d group, hypoxia 3d group, hypoxia 7d group and hypoxia 14d group. The second rats were randomly divided into control group, hypoxia group, hypoxia group + Zinc protoporphyrin (ZnPP) group. Pulmonary artery pressure was measured by right heart catheterization method; the ratio of right ventricle and left ventricle was calculated and calculated; CO content in plasma and lung homogenate of rats was measured indirectly by dual wavelength spectrophotometer; Technology The first batch of rat lung HO 1 protein expression localization and semi-quantitative analysis. Results Hypoxia began to form stable pulmonary hypertension with right ventricular hypertrophy 7 days to 14 days after hypoxia in rats. The contents of CO in plasma and lung homogenate were significantly increased at 1 and 2 days of hypoxia (P <0.01) . The expression of HO 1 in alveolar and alveolar interstitial macrophages and inflammatory cells increased after hypoxia for 1 ~ 3 h, and was significantly increased in pulmonary alveolar smooth muscle cells after hypoxia for 7 ~ 14 days (F = 8 72, P <0 0 0 1). The mean pulmonary artery pressure in hypoxia + ZnPP group was significantly higher than that in control group and hypoxia group, and the content of CO in plasma and lung homogenate was significantly lower than that in hypoxia group (all P <0.01). Conclusion The endogenous CO / HO system was significantly increased in chronic hypoxia and showed a time-dependent bimodal phenomenon. The second compensatory increase was closely related to the change of pulmonary artery pressure. The intervention of HO 1 inhibitor It further indicates that the endogenous CO / HO system is absent