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bFGF、MMP-2在肺血减少型先天性心脏病幼猪动物模型远端肺血管发育中的作用 被引量:1

Effect of bFGF and MMP-2 in the Development of the Distal Vessels in the Porcine Model of Congenital Heart Defect with Decreased Pulmonary Blood Flow
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摘要 目的:采用球囊扩张人工房间隔造口+肺动脉环缩术建立肺血减少型先天性心脏病幼猪动物模型,探讨肺血减少时远端肺血管形态学变化的病理生理机制.方法:将出生1~2个月的幼猪20头随机分为3组.对照组(C组,n=6):右胸小切口制成一过性肺血减少;轻度-中度肺动脉狭窄组(T1组,n=7):经右心房表面送入球囊扩张器,行人工房间隔造口+肺动脉Banding环缩术,控制收缩期肺动脉环缩处压差(Trans-PABP)为20~30 mmHg;重度肺动脉狭窄组(T2组,n=7):术中Trans-PABP≥30~50 mmHg.三组于术后2个月取右肺中叶外侧段1.0 cm×0.8 cm×0.8 cm大小的肺组织,光学显微镜下观察远端肺细小动脉形态学改变,并采用双抗体夹心酶联免疫吸附法(ELlSA)检测血清碱性成纤维细胞生长因子(bFGF)和基质金属蛋白酶2(MMP-2)的含量.结果:T1、T2组行房间隔造口+肺动脉环缩术均获成功.术后2个月,T1、T2两组肺细小动脉内径均大于C组(P<0.05),肺细小动脉数目(NAPSC)均少于C组(P<0.05).血清bFGF 、MMP-2含量,T1、T2两组较C组升高(P<0.05),而C组手术前后没有明显变化(P>0.05).结论:肺血减少型先天性心脏病幼猪,肺组织细胞外基质发生构型重建,肺细小血管发育不良或退化,其发生基质重塑的基础是肺血减少时引起一系列酶和细胞因子等成分的变化. Objective: To study the pathophysiological mechanism of the morphological change of immature pulmonary vessels in the piglet model of congenital heart defect with decreased pulmonary blood flow established with balloon atrial septostomy and pulmonary artery banding. Methods: Twenty piglets at an age of one to two months were divided into three groups with random number table. For the control group (group C, n = 6), small incisions were carried out on the right chest to produce a transient reduction in the pulmonary blood;For the low - medium pulmonary artery stenosis group ( group T1, n = 7 ), the balloon dilator was delivered through the surface of the right atrium and septostomy and pulmonary artery banding were performed, and the systolic transpulmonary artery banding pressure( Trans -PABP)was controlled to be 20 -30 mmHg; For the severe pul- monary artery stenosis group ( group T2, n = 7 ), the same surgical procedures with group T1 were performed while Trans - PABP was controlled to be more than 30 - 50 mmHg. At 2 months after surgery, a lung tissue of 1. 0 cm × 0.8 cm × 0.8 cm from lateral segment of the right middle lobe was taken out to be observed under optic microscope. The morphological change of the distal arterioles was detected. Furthermore, the content of basic fibroblast growth factor (bFGF)and matrix metalloproteinase -2 (MMP -2) were also examined by the method of enzyme - linked immunosorbent assay (ELISA). Results: The model was successfully established in all the survival piglets of the group T1 and group T2. Two months after operation, in group T1 and T2 the inner diameter of the pulmonary arterioles was significantly larger than that of group C ( P 〈 0.05 ), the number of arterioles per square centimeter(NAPSC) was significantly lower than that of the group C ( P 〈 0.05 ). The expression of bFGF and MMP - 2 in serum in group T1 was significantly higher than that on group C ( P 〈 0.05 ), so as group T2 (P 〈 0.01 ), But group C did not change before operation and after operation(P 〉 0.05 ). Conclusions: Structural remodeling of pulmonary extracellular matrix is an important feature of the piglet model of congenital heart defect with decreased pulmonary blood flow. The arterioles show significant hypoplasia or degradation. Change of a series of enzymes and cytokines during the reduction of blood in the lung is the key to structural remodeling.
出处 《解剖与临床》 2011年第5期404-408,共5页 Anatomy and Clinics
基金 安徽省高等学校省级重点自然科学研究项目,编号:KJ2009A74
关键词 先天性心脏病 肺血流减少 动物模型 肺小血管 碱性成纤维细胞生长因子 基质金属蛋白酶2 Congenital heart disease Reduction in the pulmonary blood Animal model Pulmonary vessel basic fibroblast growth factor Matrix metalloproteinase - 2
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