中文摘要：

目的探讨慢性低氧对大鼠肺内动脉血管重构以及5-HT诱发肺内动脉血管环收缩效应的影响。方法常压慢性低氧诱导慢性肺动脉高压大鼠模型。比较正常组（NOR组）和慢性低氧组（CH组）大鼠血流动力学参数平均右心室收缩压（mRVSP），平均右心室压（mRVP）及右心室压最大上升速率（dp／dtmax）及右心室肥厚指数以鉴定模型；光学显微镜下观察肺血管的病理改变；记录肺内动脉血管张力，观察5-羟色胺（5-HT）收缩效应；比较不同Ca^2＋通道阻断剂对5-HT引起的收缩效应的阻断作用。结果与NOR组比较，低氧3～4周后CH组的mRVSP、mRVP、dp／dtmax和右心室肥厚指数均明显增高（P〈0．01）；CH组大鼠肺内动脉中膜显著增生；CH组的5-HT引起的肺内动脉环收缩的浓度-依赖性反应曲线左移；30μmol／L氯化镧对30μmol／L 5-HT预收缩肺内动脉血管环效应的阻断作用在CH组显著增高（P〈0．01），但30μmol／L SKF96365的阻断作用无显著性意义。结论慢性低氧3～4周可稳定引起大鼠肺动脉高压，并左移5-HT诱发的肺内动脉环收缩的浓度-依赖性反应曲线；Ca^2＋池操纵性Ca^2＋通道功能的上调可能是CH组5-HT高反应性的一种机制。

英文摘要：

Objective To investigate the effect of chronic hypoxia on the vascular remodeling and contractile response to 5-HT on pulmonary arterial rings. Methods A rat pulmonary arterial hypertension model was established by chronic hypoxic exposure. The rats from normoxic （NOR） and chronic hypoxic （CH） group were assessed by measuring the hemodynamic parameters, such as RVSP, RVP and dp/ dtmax,as well as by examining the weight ratio of right ventricle to left ventricle plus septum. Moreover the pathological changes of lung sections （H-E stained） were observed under light microscope. Tension studies of PA rings by organ bath technique was introduced to observe the effect of 5-HT-induced contrac- tion on NOR and CH pulmonary arterial rings. The effect of different Ca^2＋ channel blocking agents on 5- HT-induced contraction was examined. Results After 3-4 weeks exposure to hypoxia, the mRVSP, mRVP, dp/dtmax and the weight ratio were significantly increased in CH group rats （P〈0.01）. The tunica media of pulmonary artery from CH group was significantly thickening, and in a dose-dependent man ner, a significant increase in 5-HT induced vasoconstriction response of pulmonary arterial rings can be observed from the same group. The inhibitory effect of 30μmol/L La^3＋ on precontracted rings with 30 μmol/L 5-HT was significantly increased in CH rats（P〈0.01）. However there is no significant difference for the inhibitory effect of a 30 μmol/L SKF96365 treatment between the two group rats. Conclusions A 3-4 weeks exposure to hypoxia could induce pulmonary hypertension and inerease vascular eontractile response to 5-HT. Store-operated calcium channels of pulmonary artery that up-regulated by chronic hypoxia may contribute to the hyperreactivity to 5-HT in CH-rats.