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经心肌血运重建治疗的小鼠中心肌血管生成的激活和成纤维细胞生长因子-2的上调。

Activation of myocardial angiogenesis and upregulation of fibroblast growth factor-2 in transmyocardial-revascularization-treated mice.

作者信息

Chiotti K, Choo S J, Martin S L, Reichert C, Grass T M, Duran C M, Coffin J D

机构信息

McLaughlin Research Institute, Great Falls, Montana, USA.

出版信息

Coron Artery Dis. 2000 Oct;11(7):537-44. doi: 10.1097/00019501-200010000-00004.

DOI:10.1097/00019501-200010000-00004
PMID:11023241
Abstract

OBJECTIVE

To evaluate the growth factor responses associated with myocardial angiogenesis.

DESIGN

Mice were treated with transmyocardial revascularization (TMR) and evaluated for angiogenic and growth factor responses.

METHODS

TMR was performed via thoractomy with a 27 g needle. At 2, 5, and 7 days post-treatment, hearts were removed from the TMR treated and control groups, then assayed for angiogenesis, fibroblast growth factor (FGF)-2 expression and vascular endothelial cell growth factor (VEGF) expression.

RESULTS

TMR caused an angiogenic reaction in the myocardial blood vessels at 7 days post-TMR treatment. Elevated FGF-2 corresponded with increased TMR related angiogenesis. VEGF levels only increased in hearts that were prewounded then TMR treated.

CONCLUSIONS

The data show that TMR stimulates myocardial angiogenesis. The angiogenic reaction is mediated by FGF-2 which increased in most experimental treatment groups. The VEGF response was more specific, requiring prewounding then TMR treatment for a VEGF increase.

摘要

目的

评估与心肌血管生成相关的生长因子反应。

设计

对小鼠进行经心肌血管重建术(TMR),并评估其血管生成和生长因子反应。

方法

通过开胸用27g针头进行TMR。在治疗后2、5和7天,从TMR治疗组和对照组取出心脏,然后检测血管生成、成纤维细胞生长因子(FGF)-2表达和血管内皮细胞生长因子(VEGF)表达。

结果

TMR治疗后7天,TMR引起心肌血管的血管生成反应。FGF-2升高与TMR相关的血管生成增加相对应。VEGF水平仅在预先受伤然后接受TMR治疗的心脏中升高。

结论

数据表明TMR刺激心肌血管生成。血管生成反应由FGF-2介导,在大多数实验治疗组中FGF-2增加。VEGF反应更具特异性,需要预先受伤然后进行TMR治疗才能使VEGF增加。

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