中文摘要：

目的探讨心肌内注射人源成纤维细胞生长因子2（hFGF-2）对急性心肌梗死后左心室重构的影响。方法32只SD大鼠随机均分为对照组和治疗组,建立急性心肌梗死模型,治疗组于梗死心肌周围心肌内注射重组质粒pAdTrace-hFGF2100μg,对照组给予等量生理盐水。于术后4周取心肌组织行冰冻切片、苏木素-伊红（HE）染色、Ⅷ因子染色和天狼猩红染色观察。结果术后4周时,治疗组有红色荧光蛋白表达,HE染色及Ⅷ因子染色均可见梗死心肌周围新生血管数目较对照组增多（P〈0.05）;治疗组左室壁横截面积较对照组增加（P〈0.05）,但两组左室腔大小、瘢痕心肌厚度及心肌细胞大小无显著差异;治疗组Ⅰ、Ⅲ型胶原含量与对照组比较差异无统计学意义,但Ⅰ/Ⅲ型胶原比值低于对照组（P〈0.05）。结论直接心肌内注射FGF-2可能促进血管新生,调节胶原含量及胶原比值,从而改善急性心肌梗死后的心室重构。

英文摘要：

Objective To investigate the effects of intramyocardial injection of human fibroblast growth factor-2 （hFGF-2） on left ventricular （LV） remodeling after acute myocardial infarction. Methods Thirty-two SD rats were randomly divided into treatment group and control group. A model of acute myocardial infarction was established. Rats in treatment group received intramyocardial injection of recombinant plasmid pAdTrace-hFGF2 100μg on the margin of the infarct zone, while rats in control group received injection of equal volume of saline. LV myocardial tissue was excised 4 weeks after modeling for frozen section, paraffin sections for hematoxylin-eosin （HE） stai ning, factor W staining and sirius red staining for histological evaluation. Results Four weeks after producing infarct, the red fluorescent protein was found to be expressed in treatment group. In sections with HE and factor Ⅷ staining an increased number of nascent vessels could be obviously seen around the infarct area in the treatment group as compared with the control group （ P〈0. 05）. The cross-sectional area of the LV wall was increased in treatment group compared with that in control group （P〈0. 05）, but no significant difference was found between the two groups in regard to chamber area, scar thickness and myocardial cell size. The contents of type Ⅰ and type Ⅲ colla gen were increased slightly in treatment group compared with that in control group, but without statistically significant difference. However, the collagenⅠ/Ⅲ ratio in treatment group was lower than that in control group （P〈0. 05）. Conclusions Intramyocardial injection of hFGF-2 gene may improve remodeling of LA after acute myocardial infarction by stimulating angiogenesis and regulating the collagen content and collagenⅠ/Ⅲ ratio.