摘要
目的:观察乐息平(Lacidipine)对SD大鼠缺氧性肺动脉(HPH)的防治效果,以及内皮素A型受体(ETA-R)mRNA在SD大鼠肺血管平滑肌中的表达情况,进而探讨乐息平防治HPH的作用机制与内皮素(ET)由ETA-R介导的生物学效应之间的关系。方法:实验动物分为4组:正常对照组(N)、缺氧组(H)、正常+乐息平组(N+La)、缺氧+乐息平组(H+La);用常压低氧法(氧浓度:10+0.5%)制作HPH动物模型;用插管法测定肺动脉压;用组织切片内原位杂交法检测ETA-RmRNA的表达情况。结果:缺氧组(H)平均肺动脉压(mPAP)及ETA-RmRNA的表达均高于正常组(N)(P<0.01);缺氧加乐息平组(H+La)mPAP及ETA-RmRNA的表达均无明显增高(与H组比较P<0.01;与N组比较,P>0.05)。结论:乐息平可以防止缺氧诱导的SD大鼠肺动脉压升高,同时可以抑制ETA-RmRNA在缺氧性SD大鼠肺血管平滑肌中的表达。
Objective:To investigate the mechanism of lacidipine for prevention of HPH and the biological effects mediated by ET A -R.Method:The experimental SD rats were divided into4groups:normal control group(N),hypoxia group(H),normal control with lacidipine(N+La)and hypoxia with lacidipine(H+La).The animal model of HPH was made by hypoxia of ordinary pressure.The In Situ Hybridization was used to detect the expression of ET A -R mRNA in the pulmonary vascular smooth muscle cells of the different groups of rats.Results:Both the mean pulmonary arterial pressure and the expression of ET A -R mRNA of the H group were much higher than that of the N group(P<0.01);and the pulmonary arterial pressure was decreased to normal level in H+La group compared with H group,but the the mean pulmonary arterial pressure and the expression of ETA-R mRNA of the H+La group were not obvious increased P<0.01compared with H group,P>0.05with N group).Conclusion:Lacidipine can decrease the pulmonary arterial pressure induced by hypoxia in SD rats and inhibit the expression of ET A -R mRNA in rats pulmonary vascular smooth muscle.
出处
《海南医学院学报》
CAS
2002年第4期193-197,共5页
Journal of Hainan Medical University
