缺氧性肺动脉高压发病中肺动脉平滑肌细胞增殖与凋亡变化

目的：研究缺氧性肺动脉高压发病中肺动脉平滑肌细胞增殖与凋亡变化。方法：用压缺氧法复制大鼠缺氧性肺动脉高压模型，用右心导管法测量平均肺动脉压，称量法计算右心室肥大指数，HE染色结合形态计量分析进行缺氧性肺血管重塑观察，Tunel法行肺动脉平滑肌细胞凋亡检测。结果：缺氧7d大鼠平均肺动脉压开始升高，肺动脉出现缺氧性肺血管重塑；缺氧14d及21d平均肺动脉压进一步升高，缺氧性肺血管重塑更明显，右心室肥大指数增加。对照组及缺氧3d、7d、14d、21d组肺动脉平滑肌细胞凋亡指数差异无显著意义。平均肺动脉压与WA％（血管壁横断面积与血管横断面积比值）及右心室肥大指数呈正相关，WA％与肺动脉平滑肌细胞凋亡指数之间无直线相关关系。结论：缺氧性肺动脉高压发病中肺动脉平滑肌细胞增殖同时不伴有凋亡水平的显著变化。

Pulmonary Arterial Smooth Muscle Cells Proliferation and Apoptosis in the Pathogenesis of Hypoxic Pulmonary Hypertension

Objective:To research pulmonary arterial smooth muscle cells ploliferation and apoptosis in the pathogenesis of hypoxic pulmonary hypertension. Methods:Model of chronic hypoxia-induced pulmonary hypertension rat was duplicated by normal pressure intermittent hypoxia.Mean pulmonary arterial pressure (mPAP) was determined by right-heart catheterization.Right ventricular hypertrophy index (RVHI) was calculated according to weighs of right ventricle and left ventricle plus septum. Hypoxic pulmonary vascular remodeling (HPSR) was analyzed by computer cellular image analysis system with hematoxylin-eosin staining sections. Apoptotic pulmonary arterial smooth muscle cells were labeled by Tunel method. Results:Rat mPAP hypoxia 7 days rose significantly and HPSR was shown after 7 days hypoxia.mPAP rose further and HPSR became more obviously after hypoxia 14 days, RVHI elevated significantly as well. Pulmonary arterial smooth muscle cells apoptotic index had no clear difference between control and hypoxic rat. mPAP showed positive linear correlation with WA%(ratio of vascular wall area to total vascular area)and RVHI and the coefficient of linear correlation were 0.83 and 0.54(P<0.01).Pulmonary arterial smooth muscle cells apoptotic index have no linear correlation with WA% and the coefficient of linear correlation was-0.33 (P>0.05). Conclusion:Pulmonary arterial smooth muscle cells proliferate but their apoptotic level has no marked change in the pathogenesis of hypoxic pulmonary hypertension.