摘要
目的 :探讨人酸性成纤维细胞生长因子 (aFGF)基因重组腺病毒载体 (Ad .aFGF)转染缺血心肌后促进侧支血管增生的作用。 方法 :实验用小型猪开胸于左冠回旋支 (Lcx)放置Ameroid环 ,4周后 ,将Ad .aFGF(n =7)、Ad .Null(n =6 )、PBS (n =6 )直接注射到Lcx供血区域 ,每只 10点 ,每点 10 9pfu或 10 0 μl;4周后心脏超声检测局部心功能的改善 ,体外冠状动脉造影观察侧支血管的增生 ,注射点心肌Ⅷ因子免疫组化染色检测心肌中的新生血管。 结果 :冠状动脉造影显示Ad .aFGF组较其他两组心肌中有明显的侧支血管增生 ,局部室壁功能显著提高 ;Ⅷ因子免疫组化染色显示Ad .aFGF组心肌中新生血管的密度显著高于另两组 (P <0 .0 1)。结论 :Ad .aFGF转染慢性缺血心肌后可促进侧支血管增生 。
Objective: To investigate the collateral angiogenesis induced by gene transfer of acidic fibroblast growth factor(aFGF) into ischemic myocardium. Methods: Experimental mini swines underwent thoracotomy and placement of an Ameroid constrictor on the left circumflex coronary artery. Four weeks later, Ad.aFGF( n =7), Ad.Null( n =6) and PBS( n =6) were administrated directly into the myocardium at 10 sites in the circumflex distribution areas (10 9 pfu or 100 μl). Four weeks later, local myocardial function was examined by echocardiography. After animals were sacrificed, the existence of collateral vessels was documented by Ex vivo angiograpy and the new blood vessels were showed by Factor Ⅷ immunohistochemistry staining. Results:Echocardiograph documented a significant improvement of local myocardial function in Ad.aFGF treated animals compared with Ad.Null and PBS control. Collateral vessel angiogenesis assessed by angiography was much better in Ad.aFGF group than in Ad.Null and control group( P <0.01). The circumflex artery was almost completely reconstructed in Ad.aFGF animals. The quantitation of new blood vessels was much more in Ad.aFGF group than that in the other groups. Conclusion: Our studies demonstrate that direct intramyocardial administration of Ad.aFGF results in collateral angiogenesis. Such a strategy may be useful in patients with ischemic heart disease.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2003年第3期249-251,共3页
Academic Journal of Second Military Medical University
基金
国家自然科学基金 (39970 735 )
关键词
酸性成纤维细胞生长因子
腺病毒载体
血管新生化
生理性
心肌缺血
acidic fibroblast growth factor
adenovirus vector
neovascularization,physiologic
myocardial ischemia
gene transfer
