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目的：观察西拉普利对大鼠缺氧性肺动脉高压的治疗作用。方法：应用血液动力学变化指标、循环内皮细胞（ＣＥＣ）、一氧化氮（ＮＯ）、组织丙二醛（ＭＤＡ）、血管紧张素转换酶（ＡＣＥ）测定和电子显微镜病理学观察。结果：西拉普利治疗后，肺动脉平均压（２．８５±０．２２ｋＰａ）较安慰剂组（３．５８±０．２０ｋＰａ）显著下降，ＮＯ（２４．００±４．２１ｎｍｏｌ／Ｌ）较安慰剂组（１９．８６±１．８０ｎｍｏｌ／Ｌ）显著升高（Ｐ＜０．０１），肺组织ＡＣＥ（３８．７０±４．６２Ｕ）较安慰剂组ＡＣＥ（４５．１７±４．５６Ｕ）下降显著（Ｐ＜０．０１），组织ＭＤＡ（２６．２９±４．８１ｎｍｏｌ／ｍｇ）较安慰剂组（３１．４６±３．４８ｎｍｏｌ／ｍｇ）显著下降（Ｐ＜０．０１），肺组织的病理学损伤减轻。结论：西拉普利可降低肺动脉高压，促进ＮＯ释放，减轻肺动脉内皮的病理损伤
Objective: To observe the therapeutic effect of cilazapril on hypoxic pulmonary hypertension in rats. Methods: Hemodynamic parameters, circulating endothelial cells (CEC), nitric oxide (NO), malondialdehyde (MDA), angiotensin converting enzyme (ACE) and electron microscopy were used to observe the changes. RESULTS: After Cilazapril treatment, mean pulmonary artery pressure (2.85 ± 0.22 kPa) was significantly lower than placebo (3.58 ± 0.20 kPa), while NO (24.00 ± 4.21 nmol / L) The placebo group (19.86 ± 1.80nmol / L) was significantly higher (P <0.01), the lung tissue ACE (38.70 ± 4.62U) than the placebo group (45.17 ± 4.56U ) Significantly decreased (P <0.01), tissue MDA (26.29 ± 4.81nmol / mg) decreased significantly compared with placebo group (31.46 ± 3.48nmol / mg) Histopathological damage lessened. Conclusion: Cilazapril can reduce pulmonary hypertension, promote the release of NO and alleviate the pathological injury of pulmonary artery endothelium