通过观察肺动脉高压大鼠肺动脉张开角的大小，了解卡托普利及氯沙坦对肺动脉高压大鼠肺动脉零应力状态的影响。

选取健康雄性SD大鼠(体重为350 g～400 g)40只，随机分为试验组(n＝30)和对照组(n＝10)。试验组大鼠按参照文献行左肺切除，术后第7天于项背部皮下注射野百合碱(monocrotaline，MCT)(Signa公司，美国)，剂量为60 mg/kg，建立肺动脉高压(pulmonary artery hypertension，PAH)模型。于手术后第5周(注射野百合碱后第4周)，行血流动力学检查后处死。随机从试验组中取20只大鼠，从左肺切除术前3 d起，分别给予卡托普利10 mg/(kg·d) (captopril组，n＝10)，氯沙坦15 mg/(kg·d)(losartan组，n＝10)，另外10只喂等量生理盐水(PM组，n＝10)，口服给药直至处死前2 d。对照组不做任何处理。5周后观察4组的平均肺动脉压(mean pulmonary arterial pressure，mPAP)、右心室质量，即右心室/左心室＋室间隔[RV/(LV＋S)]，通过应用计算机图像分析软件测量肺动脉张开角的方法测定大鼠肺动脉的零压力状态。

PM组平均肺动脉压为(39.62±1.46) mm Hg、右心室质量(比值)为(62.66±0.61)%，分别较captopril组[(24.38±1.19)mm Hg, (48.82±1.12)%], losartan组[(23.95±0.97)mm Hg，(49.15±1.41)%]及对照组[(17.62±1.12)mm Hg, (26.86±0.96)%]增高，差异有显著意义(P<0.001)；captopril组和losartan组比较，差异无显著意义(P>0.05)。PM组肺动脉张开角[(79.13±4.19)°]明显小于captopril组[(103.63±5.69)°]、losartan组[(102.91±5.77)°]及对照组[(139.17±4.27)°]，差异有显著意义(P<0.001)；而captopril组和losartan组比较，差异无显著意义(P>0.05)。

卡托普利及氯沙坦通过干预肺动脉零应力状态，从而缓解肺动脉高压和肺血管重构的形成。

To observe the opening angle of rats' pulmonary artery and explore effects of captopril and losartan on the zero-stress state of the pulmonary artery in rats with pulmonary artery hypertension(PAH).

Forty male Spraque-Dawley rats were average divided into 4 groups randomly which included the pulmonary artery hypertension (created by pneumonectomy plus MCT injection) model group(PM group), PAH model treated with captopril [captopril group, 10 mg/(kg·d)] or losartan [(losartan group, 15 mg/(kg·d)] and normal control(control group). Mean pulmonary arterial pressure (mPAP), weight ratio of RV to LV+ S were measured at day 35. Meanwhile, the zero-stress state characterized by opening angle of the pulmonary arterial was observed by an image processing system.

Mean pulmonary artery pressure and RV/(LV+ S) in PM group [(39.62±1.46) mm Hg, (62.66±0.61)%] increased significantly than those of captopril group [(24.38±1.19) mm Hg, (48.82±1.12)%], losartan group [(23.95±0.97)mm Hg, (49.15±1.41)%], and control group [(17.62±1.12) mm Hg, (26.86±0.96)%] (P<0.001). Opening angle in PM group [(79.13±4.19)°] decreased significantly than those of captopril group[(103.63±5.69)°], losartan group [(102.91±5.77)°], and control group[(139.17±4.27)°] (P<0.001). Mean pulmonary artery pressure, RV/(LV+ S) and opening angle in captopril group and losartan group had no significant difference (P>0.05).

Captopril and losartan induced attenuation of pulmonary artery pressure and associated pulmonary vascular remodeling are likely related to their action on the regulation of the zero-stress state of the pulmonary artery in rats.