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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。
OBJECTIVE: To detect the changes of pulmonary collagen type Ⅰ and Ⅲ in chronic heart failure, observe the ultrastructure changes of pulmonary vascular endothelial cells, and evaluate the intervention of fosinopril and losartan. Methods: Eighteen patients with chronic heart failure (LVEF <45%) were divided into five groups: fosinopril group (HFF group), losartan group (HF-L group) Sodium chloride solution group (HF-C group) (7), another set of sham operation group (6). Eight weeks after the drug treatment, the mean pulmonary arterial pressure (mPAP) was measured by right heart catheterization, and the contents of type I and type III collagen in pulmonary vessels were detected by picric red staining. The ultrastructure of pulmonary arterioles were observed by electron microscopy. Results: Compared with the sham operation group, the mPAP of HF-C group was significantly higher than that of the sham operation group [(17.5 ± 4.6) vs (28.9 ± 5.8) mmHg (1mmHg = 0.133kPa, P <0.05] The mPAP was significantly lower in the HF-F and HF-L groups (28.9 ± 5.8 vs. 21.6 ± 5.0 mmHg, 28.9 ± 5.8 and 20.5 ± 4.9, respectively, P <0.05). Compared with the sham-operation group, the content of type I and type III collagen in pulmonary vessels increased significantly in HF-C group [(11.76 ± 3.65)% vs (19.07 ± 6.13)%, P <0.05] (19.07 ± 6.13)%: (12.72 ± 4.03)%, (19.07 ± 6.13)%: (12.72 ± 4.03)% in HF-F group and HF-L group, P <0.05]. The structure of lung tissue was normal in sham-operated group, the endothelial cells of pulmonary arteriole were swollen, mitochondria were swollen, vacuolization and crest lysis, the endoplasmic reticulum was dilated, subepithelial edema, middle muscular pulmonary artery hypertrophy and collagen fiber were dense in HF- The changes of pulmonary vascular structure in group F and HF-L were significantly reduced. CONCLUSIONS: Pulmonary vascular remodeling and elevated mPAP occur during heart failure. Fosinopril and losartan inhibit pulmonary vascular remodeling and decrease mPAP.