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目的研究野百合碱(MCT)诱导肺动脉高压(PH)大鼠肺动脉Ⅰ型胶原的变化,探讨肺血管结构重建的机制。方法雄性Wistar大鼠12只,随机分为MCT组(n=6)和对照组(n=6)。MCT组腹腔注射MCT(60 mg.kg-1,第1天),对照组注射同等剂量9 g.L-1盐水。实验3周后,测定各组平均肺动脉压(mPAP)、右心室/(左心室+室间隔)比值[RV/(LV+S)]、大鼠体质量;光镜下观察其肺组织HE染色结果,免疫组织化学法检测其肺动脉Ⅰ型胶原蛋白的表达,并进行定位和半定量分析。应用SPSS 13.0软件进行统计学分析。结果与对照组比较,MCT组大鼠mPAP及RV/(LV+S)显著升高[mPAP:(10.60±2.06)mmHg(1 mmHg=0.133 kPa)vs(32.40±3.24)mmHg,P<0.01;RV/(LV+S):0.28±0.04vs0.47±0.10,P<0.01],体质量显著减低[(291.4±11.6)gvs(252.7±6.8)g,P<0.01];光镜下可见MCT组大鼠肺动脉血管内皮细胞出现肿胀、坏死、脱落;肺动脉平滑肌明显增生,管壁明显增厚,管腔狭窄,甚至闭塞,肺血管结构发生重建;MCT组肺中小动脉Ⅰ型胶原表达均显著升高(中动脉:0.23±0.01vs0.27±0.02,P<0.01;小动脉:0.24±0.01vs0.30±0.02,P<0.01)。结论肺动脉中Ⅰ型胶原堆积是MCT诱导PH大鼠肺血管结构重建的重要组成部分。
Objective To study the changes of pulmonary collagen I in pulmonary arterial hypertension (PH) induced by monocrotaline (MCT) in rats, and to explore the mechanism of pulmonary vascular structural remodeling. Methods Twelve male Wistar rats were randomly divided into MCT group (n=6) and control group (n=6). The MCT group was intraperitoneally injected with MCT (60 mg.kg-1 on the first day), and the control group was injected with the same dose of 9 g.L-1 saline. After 3 weeks of the experiment, the mean pulmonary artery pressure (mPAP), right ventricle/(left ventricle + ventricular septum) ratio [RV/(LV+S)], and body weight of the rats were determined; HE staining of the lung tissues was observed under a light microscope. As a result, the expression of type I collagen in pulmonary artery was detected by immunohistochemical method, and localization and semi-quantitative analysis were performed. SPSS 13.0 software was used for statistical analysis. Results Compared with the control group, mPAP and RV/(LV+S) increased significantly in the MCT group [mPAP: (10.60±2.06)mmHg (1 mmHg=0.133 kPa) vs (32.40±3.24) mmHg, P<0.01; RV/(LV+S): 0.28±0.04vs0.47±0.10, P<0.01 ], body mass was significantly reduced [(291.4±11.6) gvs (252.7±6.8) g, P<0.01]; MCT was seen under light microscope Pulmonary arterial endothelial cells were swollen, necrotic, and detached; pulmonary artery smooth muscles were significantly proliferated, with thicker walls, narrow lumens, and even occlusion. Pulmonary vascular structures were reconstructed; expression of type I collagen in the pulmonary arterioles was significantly increased in the MCT group. High (medium artery: 0.23±0.01 vs 0.27±0.02, P<0.01; arteriole: 0.24±0.01 vs 0.30±0.02, P<0.01). Conclusion Type I collagen accumulation in pulmonary artery is an important part of pulmonary vascular remodeling induced by MCT in PH rats.