血管内皮生长因子促进慢性心肌梗死血管生成

Vascular Endothelial Growth Factor Promote Angiogenesis in Chronic Myocardial Infarction

目的探索血管内皮生长因子对猪慢性心肌梗死的治疗作用。方法通过开胸直视下结扎前降支建立猪的心肌梗死模型,1个月后将建模成功的猪分为血管内皮细胞生长因子(VEGF)组和对照组,分别直视下心肌内注射VEGF和磷酸缓冲盐溶液(PBS),2个月后行MR检查比较两组心功能参数,梗死心肌组织分别做HE染色和免疫组化染色,分析梗死区域微血管生成和细胞增殖情况。结果因子注射2个月后,两组干预前后的心功能指标差值比较分别为左心室射血分数(LVEF)(4.0%±10.4%vs 1.8%±1.6%,P>0.05)、心排出量(CO)(2.1±1.6L/min vs 1.4±0.8L/min,P>0.05)、左心室后壁舒张期厚度(LVPWTd)(2.8±0.5mm vs 2.0±0.8mm,P>0.05)、左心室舒张末期容积(EDV)(24.0±5.0ml vs 39.6±16.2ml,P>0.05)。通过免疫组化染色分析,VEGF组的微动脉密度比对照组高(87.0±9.1 vs 50.8±7.2,P<0.05),毛细血管密度比对照组高(367.5±50.8 vs 188.5±14.3,P<0.05),增殖细胞核数目较对照组多(432.5±37.7 vs 132.0±29.0,P<0.05)。结论VEGF能够促进梗死心肌的血管新生,促进梗死区域侧支循环建立。

Objective To explore the effect of vascular endothelial growth factor for swine with chronic myocardial infarction. Meth- ods Swine were modeled myocardial infarction through ligating the left anterior descending artery by thoraeotomy. Modeled swine were di- vided into VEGF group and control group. The VEGF protein was injected into the myocardium around the infarcted area by thoracotomy in VEGF group, while PBS in control group. After two months, the heart function of the two groups were evaluated and compaired by MR, and vascularization and cell proliferation were analysed by HE stain and immunohistochemisty stain. Results After two months, the difference comparisons of the two groups before and after treatment about indexes of heart function were LVEF（4.0% ± 10.4% vs 1.8%± 1.6% ,P 〉 0.05 ） , CO （2.1±1.6L/rain vs 1.4 ±0.8L/rain, P 〉 0.05 ） , LVPWTd （ 2.8± 0.5mm vs 2.0± 0.8mm, P 〉 0.05 ） , EDV （ 24.0 ± 5.0ml vs 39.6± 16.2ml,P 〉0.05）, respectively. Moreover, not only the arterioles density and the capillary density of the VEGF group were higher than the control group （87.0 ± 9.1 vs 50.8 ± 7.2 and 367.5± 50.8 vs 188.5 ± 14.3, respectively, P 〈 0.05 ） , but also proliferating cell nuclear numbers were more （432.5 ±37.7 vs 132.0 ± 29.0, P 〈 0. 05 ） according to the immunohistochemisty assay. Conclusion VEGF can facilitate angiogenesis in the infarcted myocardium, as well as formation of the collateral circulation.