雌激素对低氧性肺血管重建的作用

The effects of estrogen on hypoxic pulmonary vascular remodeling

目的观察17-β雌二醇对低氧性肺动脉高压大鼠肺血管重建的作用。方法采用间断常压低氧法建立大鼠低氧性肺动脉高压模型,以右心导管法测定肺动脉压力(mPAP);测定右心室肥厚指数[RV/(LV+S)];肺组织切片采用HE染色,经图像分析技术测定大鼠肺小血管管壁厚度指标[管壁厚度与血管外径的百分比(WT%)和管壁面积与血管总面积的百分比(WA%)];用放射免疫法测定血清中17β雌二醇浓度。将24只SD大鼠随机分成正常对照组、低氧组、雌激素预防组(每天低氧前腹腔注射17β雌二醇30μg/kg,共3周)、雌激素治疗组(低氧3周后每天腹腔注射17β雌二醇30μg/kg,共7d)。结果(1)低氧组大鼠的mPAP、RV/(LV+S)(%)、WT%和WA%均高于正常对照组(P<001);血清中17β雌二醇浓度与正常对照组比较无显著性差异(P>005)。(2)雌激素预防组、雌激素治疗组的大鼠mPAP、RV/(LV+S)(%)、WT%和WA%均低于低氧组(P<005),而血清中17β雌二醇浓度高于低氧组和正常对照组(P<001)。结论17β雌二醇能有效降低低氧性肺动脉高压大鼠的肺动脉压力、阻抑右心室肥厚,对低氧性肺动脉高压血管重建具有预防和治疗作用。

Objective To observe the effects of 17 β estradiol (E 2 ) on hypoxic pulmonary vascular remodeling.Methods Twenty four male SD rats were randomly divided into four groups:control group,hypoxic group,E 2 preventive group,and E 2 treatment group.The animal model of hypoxic pulmonary hypertension was established by regular exposing the rats to normabaric hypoxic conditions for 3 weeks.The mean pulmonary artery pressure (mPAP) and right ventricle hypertrophy index were examined.Lung speciments were examined by light microscopes and morphometric analysis.The WT% (ratio of vascular wall thickness to vascular external diameter) and WA% (ratio of vascular wall area to total vascular area) were measured by a computerized image analyzer.E 2 in blood serum was measured by radioimmunoassay.Results (1)In the hypoxic group,mPAP,RV/(LV+S),WT% and WA% were increased significantly compared with those in the control group ( P <0 01).However,E 2 level in the serum in the hypoxic rats was not significantly different from that in the control rats( P >0 05).(2)In the preventive and treatment groups,mPAP,RV/(LV+S),WT%,and WA% decreased remarkably as compared with those in the hypoxic group,respectively ( P <0 05).E 2 levels in the serum in the preventive and treatment groups were higher than that in the hypoxic group ( P <0 01).Conclusion 17 β estradiol may have the preventive and therapeutic effects on the hypoxic pulmonary vascular remodeling.