机构地区:[1]北京大学第一医院儿科,北京100034 [2]教育部分子心血管重点实验室,北京100034
出 处:《实用儿科临床杂志》2010年第1期18-20,共3页Journal of Applied Clinical Pediatrics
基 金:国家自然科学基金(30630031;30821001);国家重点基础研究发展规划项目(2006CB503807);国家长江学者奖励计划项目
摘 要: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 examine the expression of type Ⅰ collagen in pulmonary arteries of rats with monnerotaline(MCT) - induced pulmonary hypertension (PH) and explore the mechanism of puhnonary vascular structural remodeling. Methods Twelve mate Wistar rats were randomly divided into 2 groups: the MCT group( n = 6) and the control group( n = 6 ) ,which received a single intraperitoneal injection of MCT solution ( 60 mg · kg^-1, the first day ) or 9 g · L ^-1 saline, respectively. After 3 weeks, mean of pulmonary artery pressure ( mPAP), the value of right ventricle/ ( left ventricle plus septum) [ RV/ ( LV + S) 1 and body weight were measured. Lung sections ( HE stained) were observed under lightmicroscope for changes of the pulmonary arteries. The protein expression of type Ⅰ collagen in pulmonary arteries was detected by immunohistoehemical technique. Results Three weeks after MCT injection,compared with control group, mPAP and RV/ ( LV + S) increased significantly in 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 ±0.04) vs (0.47 ±0.10) ,P 〈0.01] ;The body weight in rats of MCT group was significantly lower [(291.4 ± 11.6) g vs (252.7 ± 6.8) g,P 〈0.01 ]. Damages in vascular endothelial cells of pulmonary arteries of rats received MCT injection were observed and showed hy- perplasy of smooth muscle. Lumens of arteries were narrnwed,even occluded,and the normal structure of artery wall was remodeled. The protein expression of type [ collagen in medium - sized puhnonary arteries and arterioles were both significantly higher in rats of MCT group than those of control group ( medium - sized artery : 0.23 ± 0.01 vs 0. 27 ± 0.02, P 〈 0.01 ; small - sized artery : 0.24 ± 0.01 vs 0. 30 ± 0.02, P 〈 0.01 ). Conclusions Accumulation of pulmonary artery collagen, one of the pathologic features of pulmonary vascular remodeling, contributed a great deal to
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