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应用低O_2高CO_2性肺动脉高压大鼠模型,结果表明,随低O_2高CO_2时间延长,平均肺动脉压(mPAP)与血浆内皮素(ET)进行性子行升高,呈显著正相关(r=0.742,P<0.00J1;同时平均肺细小动脉中膜厚度(mMTPA)、肺细小动脉管壁面积/管总面积(WA/TA)、肺细小动脉管腔面积/管总面积(EA/TA)。直径小于100μm肌型肺动脉数/肺动脉总数(TWPV)和平均肺动脉密度(mDPA)等定量显微形态学指标也呈同样阶梯式变化,且与ET、mPAP均有显著的正相关(P<0.05,P<0.01或P<0.001)。表明低O_2高CO_2能引起血浆ET升高,其致肺动脉平滑肌细胞增生的作用,造成一系列肺细小动脉结构改建是形成肺动脉高压的重要中间环节。
The results showed that the mean pulmonary arterial pressure (mPAP) and plasma endothelin (ET) increased significantly with the increase of low O_2 high CO_2 time (r = 0.742 , P <0.00J1; mean mean pulmonary arteriolar thickness (mMTPA), pulmonary arteriolar wall area / total tumor area (WA / TA), pulmonary arteriolar luminal area / total tumor area (EA / TA). Quantitative micromorphological indexes such as muscular pulmonary artery diameter / total pulmonary artery (TWPV) and mean pulmonary arterial density (mDPA) with diameter less than 100μm also showed the same stepwise changes, and had significant positive correlation with ET and mPAP (P <0.05, P <0.01 or P <0.001), indicating that low O_2 high CO 2 can cause elevated plasma ET, which leads to the proliferation of pulmonary artery smooth muscle cells, resulting in a series of structural remodeling of pulmonary arterioles is an important intermediate link in the formation of pulmonary hypertension.