中文摘要：

目的 研究k阿片受体激动剂（US0488H）对低氧性肺动脉高压（HPH）大鼠体内一氧化氮（NO）、内皮素（ET）及血管紧张素Ⅱ（AngⅡ）等血管活性物质水平的影响，初步探讨其防治HPH的作用机制。方法将实验动物随机分为正常对照组、低氧2周组、低氧2周＋生理盐水组及低氧2周＋US0488H组，采用低压低氧法建立大鼠HPH动物模型。2周后收集大鼠动脉血和肺组织，检测不同标本中血管活性物质NO、ET和AngⅡ水平。结果慢性低氧2周后，大鼠血清及肺组织中NO水平显著降低，而血浆及肺组织中的ET和AngⅡ水平则显著升高（P〈0．01）。U50488H可明显升高HPH大鼠血清及肺组织NO水平，同时显著降低HPH大鼠血浆及肺组织中的ET和AngⅡ水平（P〈0．01）。结论 US0488H可调节HPH大鼠体内的血管活性物质水平，其有可能通过刺激血液及肺组织NO的分泌，抑制ET和AngⅡ的产生来实现对HPH的防治作用。

英文摘要：

AIM To study the effects of U50488H on the contents of NO, ET and Ang II in HPH rats and to explore the mechanisms underlying the preventive and therapeutic effects of U50488H on hypoxic pulmonary hypertension （HPH）. METHODS Thirty-two rats randomly received one of the following treatments： normoxia control, 2w hypoxia, 2w hypoxia ＋ normal saline and 2w hypoxia ＋ U50488H. The rats were exposed to low-pressure and low-oxygen condition in an auto-modulating hypobaric and hypoxic cabin （air pressure 50 kPa） to establish HPH animal model. After 2 weeks of chronic hypoxia, concentrations of NO, ET and Ang II in blood and the contents in lung tissues were detected by nitrate reductase assay or radio immunoassay. RESULTS After 2 weeks of chronic hypoxia, NO level decreased while ET and Ang Ⅱ levels increased remarkably in both blood and lung tissues（P 〈0.01 ）. In 2w hypoxia ＋ U50488H group, the concentration of NO was higher and the concentration of ET and Ang Ⅱ were lower than those of 2w hypoxia group（P 〈 0.01 ）. CONCLUSION U50488H significantly increases NO content and decreases ET and Ang Ⅱ contents in both blood and pulmonary tissues of HPH rats. It may be one of the mechanisms underlying the preventive and therapeutic effect of U50488H on HPH.