VEGF在大鼠心肌梗死急性期表达的意义及蜕皮甾酮的促侧支循环作用  

Express of vascular endothelial growth factor in rat myocardium with AMI and the significance and effect of ecdysterone

作　　者：晋军[1] 黄岚[1] 祝善俊[1] 向常青[1] 李洪[1] 耿建萌[1] 吴旭[1] 

机构地区：[1]第三军医大学新桥医院心内科,重庆市400037

出　　处：《中国介入心脏病学杂志》2002年第3期158-161,共4页Chinese Journal of Interventional Cardiology

摘　　要：目的　以急性心肌梗死大鼠为模型 ,观察血管内皮生长因子 (VEGF)在心肌中的表达 ,探讨急性缺血缺氧刺激与VEGF产生的关系和意义以及蜕皮甾酮 (EDSecdysterone)的促侧支循环作用。方法　建立Wistar大鼠急性心肌梗死模型 ,分为对照组、急性心肌梗死组 (1、3、7d)和蜕皮甾酮干预治疗组 (每只 0 ,40mg d)。免疫组化检测VEGF表达 ;Ⅷ因子相关抗原标记内皮细胞 ,检测毛细血管密度 ,比重法测定梗死面积。原代培养大鼠心肌细胞 ,在常氧与缺氧状态下实验组分别给于蜕皮甾酮治疗 (10 0 μg ml) ,2 4h后采用免疫细胞化学法检测心肌细胞中VEGF表达。 结果　随缺血缺氧时间的延长心肌产生的VEGF增加 ,与对照组比较各组均有显著差异 ,缺血时间与VEGF产生量呈正相关 ;蜕皮甾酮治疗组与对照组相比 ,血清肌酸激酶同功酶 (CK MB)显著降低 (P <0 0 1) ;毛细血管密度增加(P <0 0 1) ;心肌梗死面积减少 (P <0 0 1)。在常氧与缺氧状态下 ,蜕皮甾酮治疗组心肌细胞VEGF表达显著高于对照组 (P <0 0 1)。结论　在心肌梗死急性期缺血心肌通过分泌VEGF对自身产生重要的保护作用 ;蜕皮甾酮进一步刺激心肌分泌产生VEGF ,促进大鼠缺血区血管生成、侧支循环建立、毛细血管密度增加 ,发挥心肌保护作用。Objective To determine the relationship and significance between the acute ischemia, hypoxia and the production of VEGF in rat myocardium and the influence of EDS on expression of VEGF protein in myocardium Methods To establish the model of AMI in rats, Wistar rats were randomly divided into control group, AMI group (1,3,7 day) and EDS group (0, 40 mg/day) Myocardial enzymes, VEGF protein, microvascular density and infarct size were detected Rat cardiac myocytes cultured primarily received EDS 100 μg/ml in normal and hypoxia condition After 24 hours, VEGF was detected with immunohistochemical technique Results The production of VEGF was higher with ischemia and hypoxia time, the positive relationship was found between the time of AMI and the production of VEGF EDS reduced the concentration of serum myocardial enzymes (CK MB), enhanced the formation of collateral circulation,microvascular density and cardiac function; decreased infarct size In addition, EDS could enhance expression of VEGF protein in cardiac myocytes of rat in normal and hypoxia condition Conclusion Acute ischemia strongly stimulated the production of VEGF in myocardium, which played an important role for autoprotection of ischemic myocardium EDS could promote the establishment of cardiac collateral circulation and enhance microvascular density in infarct zone by upregulation of VEGF protein expression

关 键 词：急性心肌梗死 血管内皮生长因子 蜕皮甾酮 侧支循环 动物模型 

分 类 号：R542.22[医药卫生—心血管疾病]