腺苷对兔缺血再灌注心肌和ET-1作用的研究

Study on Effects of Adenosine on Myocardium and Endothelin-1 during Ischemia-Reperfusion Injury in Rabbits

目的评价腺苷对缺血再灌注心肌的作用和对ET-1的影响,探讨腺苷预处理对缺血再灌注心肌保护作用的可能机制。方法家兔24只,随机分成对照组、腺苷预处理组、腺苷治疗组,每组8只。冠状动脉结扎40min,再灌注3h制备缺血再灌注模型。测定缺血前和再灌注3h后血CK的变化和心肌梗死区重量的大小,比较各组再灌注3h后SOD和MDA的变化。采用放免法测定结扎冠脉前,再灌注时,再灌注后30、60、120min血浆ET-1的变化。结果与对照组和腺苷治疗组相比,腺苷预处理组在再灌注3h后血清中CK、SOD、MDA的水平降低(P<0.01),心肌梗死面积明显减少(P<0.01);与对照组和腺苷治疗组相比,腺苷预处理组除结扎冠脉前,其余时间点ET-1的水平明显降低(P<0.01)。结论腺苷预处理可减轻再灌注损伤,对缺血再灌注心肌具有明显的保护作用,腺苷可能通过保护内皮细胞减少血浆ET-1的水平,减轻缺血再灌注损伤。

Objective To evaluate the effects of adenosine on myocardium and endothelin-1（ET-1） during ischemia-reperfusion injury in rabbits in order to explore the myocardioprotective effect and mechanism of pretreatment of adenosine during ischemia-reperfusion.Method Twenty-four healthy rabbits were randomly divided into 3 groups（8 rabbits each）：control group,adenosine pretreatment group and adenosine treatment group.Myocardial ischemia-reperfusion models were made by means of ligating the left anterior descending branch of coronary artery for 40 minutes,followed by 3 hours of reperfusion.The level of creatine kinase（CK） and the weight of infarct myocardium were detected before ischemia and after 3 hours of reperfusion.The levels of superoxide dismutase（SOD）,malonaldehyde（MDA） in each group were also compared.The plasma levels of ET-1 were measured with an immnoradiometric assay before ischemia,during reperfusion as well as 30,60,120 minutes after reperfusion.Results Compared with control group and adenosine treatment group,the levels of CK,SOD,MDA in adenosine pretreatment group significantly reduced（P〈0.01） after 3 hours of reperfusion,the infarct size significantly reduced（P〈0.01）,the levels of ET-1 were significantly lower（P〈0.01） except before ischemia.Conclusions Adenosine pretreatment can reduce the ischemia-reperfusion injury.It has significant protective effects on ischemia-reperfusion myocardium.Adenosine may reduce the level of ET-1,protect endothelial cells and reduce the ischemia-reperfusion injury.