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本实验对慢性减压缺氧（５０００ｍ）过程中肺动脉ＡＣｈ内皮依赖性舒张反应作了动态观察，并结合分析了其与内皮超微结构和肺动脉压演变的关系。结果表明，缺氧３─２１ｄ，平均肺动脉压（ｍＰＡＰ）显著递增（Ｐ＜０．０５─０．００１），而缺氧４０ｄ组基本与缺氧２１ｄ组持平，未再进一步升高。缺氧１ｄ组，各ＡＣｈ浓度（１０－１０、１０－９、１０－７、１０－６、１０－５ｍｏｌ／Ｌ）引起的内皮依赖性舒张反应明显受抑（Ｐ＜０．０５─０．００１）。缺氧７ｄ组，舒张反应的受抑程度与缺氧１ｄ组基本相同；但ＡＣｈ１０－５ｍｏｌ／Ｌ引发的反应则较缺氧１ｄ时更弱。缺氧２１ｄ和４０ｄ组，ＡＣｈ１０－６和１０－５ｍｏｌ／Ｌ引起的舒张反应，尽管仍显著低于对照，但却基本上高于缺氧１ｄ和７ｄ组。其余各浓度ＡＣｈ引发的反应则已趋于恢复至对照水平。电镜观察，缺氧１─１４ｄ肺动脉内皮呈逐渐加重的水肿变性；缺氧２１─４０ｄ内皮水肿消失，代之出现渐趋活跃的内皮增生。结果提示，随缺氧时间延长，因内皮从损伤逐渐加重到出现代偿适应，可能存在相应的内皮舒张因子由释放减少到有所恢复的动态变化过程，并对整体肺动脉压有一定程度的影响。
In our experiment, the endothelium-dependent relaxation of ACh in pulmonary arteries during chronic hypobaric hypoxia (5000m) was dynamically observed, and the relationship between it and endothelial ultrastructure and pulmonary arterial pressure evolution was analyzed. The results showed that the average pulmonary arterial pressure (mPAP) increased significantly in hypoxia from 3 to 21 days (P <0.05 to 0.001), while the level of hypoxia in 40 days was almost the same as hypoxia in 21 days, and did not increase further. Hypoxia 1d group, the concentration of ACh (10-10,10-9,10-7,10-6,10-5 mol / L) caused by endothelium-dependent relaxation was significantly inhibited (P <0.05 ─ 0. 001). In 7d hypoxia group, the degree of inhibition of relaxation was almost the same as that in hypoxia 1d group; however, the response induced by ACh 10-5mol / L was weaker than that of 1h hypoxia. The diastolic responses induced by hypoxia for 21d and 40d, ACh10-6 and 10-5mol / L were still significantly higher than those of hypoxia for 1d and 7d although they were still significantly lower than those of control. The rest of the concentration of ACh-induced reaction has tended to return to the control level. Electron microscopy showed that the endothelium of pulmonary arteries gradually degenerated from 1 day to 14 days hypoxia. Endothelial edema disappeared 21 to 40 days after hypoxia, and endothelial cells gradually became more active. The results suggest that with the prolonged hypoxia time, the endothelium gradually aggravates from injury to compensatory adaptation, there may be a corresponding dynamic change of the release of endothelium from the release to recovery, and the overall pulmonary arterial pressure to a certain extent .