中文摘要：

目的：检测慢性心力衰竭时肺血管Ⅰ型和Ⅲ型胶原含量变化,观察肺血管内皮细胞超微结构改变,并评价福辛普利及氯沙坦对其的干预作用。方法：18只慢性心力衰竭（LVEF〈45%）大鼠分为福辛普利组（HF-F组）（5只）、氯沙坦组（HF-L组）（6只）、0.9%氯化钠溶液组（HF-C组）（7只）,另设假手术组（6只）。药物治疗8周后,右心导管测量肺动脉平均压（mPAP）,苦味酸天狼猩红溶液染色-偏振光显像检测肺血管Ⅰ型和Ⅲ型胶原含量,电镜观察肺小动脉超微结构改变。结果：与假手术组比较,HF-C组大鼠mPAP显著升高[（17.5±4.6）∶（28.9±5.8）mmHg（1mmHg=0.133kPa）,P〈0.05];与HF-C组比较,HF-F组和HF-L组mPAP显著降低[（28.9±5.8）∶（21.6±5.0）mmHg,（28.9±5.8）∶（20.5±4.9）mmHg,P〈0.05]。与假手术组比较,HF-C组大鼠肺血管的Ⅰ型和Ⅲ型胶原含量显著增加[（11.76±3.65）%∶（19.07±6.13）%,P〈0.05];与HF-C组比较,HF-F组和HF-L组肺血管Ⅰ型和Ⅲ型胶原含量显著减少[（19.07±6.13）%∶（12.72±4.03）%,（19.07±6.13）%∶（12.72±4.03）%,P〈0.05]。假手术组肺组织结构正常,HF-C组肺小动脉内皮细胞肿胀,线粒体肿胀、空泡化和嵴溶解,内质网扩张,内皮下水肿,肌性肺动脉中层肥厚,胶原纤维密集;HF-F组和HF-L组肺血管结构的变化明显减轻。结论：心力衰竭时存在肺血管结构的重建和mPAP升高,福辛普利和氯沙坦治疗抑制肺血管结构重建,并降低mPAP。

英文摘要：

Objective：To detect collagen in pulmonary artery and to observe the structural remodeling of pulmonary artery of rats with chronic heart failure, and to evaluate the effect of long-term treatment with fosinopril and losartan. Method：There were eighteen rats with LV ejection fraction 〈45% randomized to four groups： ① HF-F（n=5） （fosinopril, 50 mg·kg^-1 · d^-1）, ②HF-L（n=6） （losartan, 30 mg · kg^-1 · d^-1）, ③HF-C（n=7） （placebo）,④sham-operated rats （n=6）. After 8 weeks of treatment, mean pumonary artery pressure （mPAP） was measured with catheterization. The pulmonary artery was stained with picrosirius red, and then the slices were measured under a light microscope with a linear polarization unit. The ultrastructural changes in intra-acinar pulmonary muscularized arteries were observed by transmission electron micrograph. Result： Compared with that of sham-operated rats, mPAP of HF-C was significantly increased （[17.5±4.6] ： [28.9±5.8]mmHg, P〈0. 05）. Compared with that of HF-C, mPAP of HF-F and HF-L （[28.9±5.8] ： [21.6±5.0]mmHg, [28.9±5.8] ： [20.5±4.9]mmHg, P〈0.05） were significantly decreased. Compared with that of sham-operated rats, collagen was significantly increased in pulmonary artery（[11. 76±3.65]% ： [19.07±6.13]%, P〈0.05） of HF-C. Compared with that of HF-C, collagen in pulmonary artery of HF-F and HF-L （[19.07±6. 13]% ： [12.72±4.03]%, [19.07±6. 13]% ： [12.72±4. 031%, P〈0. 05） was significantly decreased. Conclusion： The mPAP and pulmonary vascular structural remodeling are increased during chronic heart failure, which fosino-pril and losartan can prevent.