中文摘要：

目的：研究等长收缩运动诱导的生理性缺血训练促进心肌缺血模型外周血VEGF表达的时间规律。方法：健康成年新西兰兔23只,体重2.5±0.5kg。于坐骨神经外膜纵行植入电极,施加高强度脉冲电刺激（40Hz、1ms、2.5mA）,诱发靶肌肉（腓肠肌）等长收缩运动,作为生理性缺血训练的模型;在冠状动脉左室支安装气囊梗阻器,制作可控性心肌缺血模型。造模成功后随机分为假手术组（SO）、单纯心肌缺血组（MI）和生理性缺血训练组（PI）。缺血负荷为2min/h、2次/d,共4周;PI组为每次训练5min,休息5min,重复8次/d,共4周。各组分别于实验前和实验后第1、2、3和4周耳中动脉取血,采用ELISA技术检测血液中VEGF浓度。结果：SO外周血VEGF各时间点差异无显著性意义（P〉0.05）;MI和PI实验后各时间点均较实验前表达升高（P〈0.05）,第2周外周血VEGF的表达达到高峰,之后进入平台期。第1、2、3、4周各组两两比较差异均有显著性（P〈0.05）。结论：骨骼肌生理性缺血训练可以提高外周血VEGF的含量,在第2周达高峰,之后进入平台期,其VEGF升高超过单纯心肌缺血训练。

英文摘要：

Objective：To determine the time course of circulating serum VEGF promoted by myocardial ischemia and physiological ischemic training.Method：Twenty-three New Zealand rabbits were subjected to brief occlusion of left ventricle coronary artery branch（LVB） .The myocardial ischemia model was the LVB occlusion with a balloon occluder for 2min,repeated twice a day for 4 weeks.After myocardial ischemia models were successfully completed,electrode from a pulse electrical stimulator was anchored in sciatic nerve of hindlimb.The hindlimb underwent 5 min electrical stimulation（40Hz,2.5mA） followed by 5min rest,which was repeated 8 times/d for 4 weeks.The subjects were randomly divided into sham operation group（SO） ,myocardial ischemia group（MI） and physiological ischemic training group（PI） .Blood samples were collected at baseline and the 1st,2nd,3rd and 4th week from each group.Serum VEGF concentrations were measured using ELISA kit.Result：VEGF increased significantly in MI and PI,which reached peak at the end of 2nd week（P〈0.01） .Both MI and PI have no significant difference at the 2nd,3rd and 4th week（P〉0.05） .The circulating serum VEGF level increased significantly in MI at all time points during experiment comparing with SO（P〈0.01） .Serum VEGF in PI was higher than that in MI after physiological ischemic training（P〈0.05） .Conclusion：The peak VEGF expression occurred in the end of 2nd week after 4-week training in PI.Physiological ischemic training may increase the expression of circulating serum VEGF over the effect of pure myocardial ischemia.