布托啡诺后处理对缺血再灌注损伤大鼠心肌炎性因子的影响

目的 观察布托啡诺后处理对缺血再灌注损伤大鼠心肌炎性细胞因子的影响及其机制.方法 采用结扎冠状动脉前降支30min、开放120min的方法 建立心肌缺血再灌注损伤模型.健康SPF级成年雄性wistar大鼠50只,随机分为5组(n=10).A组:假手术组;B组:I/R组;C组:布托啡诺后处理组;D组:布托啡诺联合选择性κ...

The Effects of Butorphanol Postconditioning on Myocardial Factor of Rats with Ischemical Reperfusion Injury

Objective To explore the effects of butorphanol postconditioning on myocardial factor of rats with ischemical and reperfusion injury and its potential mechanism.Methods The model of ischemical reperfusion injury was established by ligation of ligation of left anterior coronary descending branch(LAD) for 30 mins and removing the ligation for 120 mins.Fifty anesthetized adult male rats were randomly divided into five groups(n=10):Group A(sham group),left anterior coronary descending(LAD) branch only exposed but not ligated for 120 mins;Group B(I/R group),ligation of LAD branch for 30 mins and removing the ligation for 120 mins and Sodium Chloride(5 ml/kg) was given intravenously 5 mins before the reperfusion;Group C(butorphanol postconditioning group),butorphanol 50 μg/kg was given intravenously 5 mins before the reperfusion,others being the same as in group B;Group D(butorphanol combined with Nor-BNI group),being the same as Group C,but Nor-BNI(2 mg/kg) was given intravenously 2 mins before the reperfusion;Group E(butorphanol combined with glibenclamide group),the same as group C too,but glibenclamide(1 mg/kg) was given intravenously 2 mins before the reperfusion.At the end of the experiment,the myocardial infarcts were examined by using TTC staining.Plasma TNF-α and IL-6 were measured after 120 mins of reperfusion respectively.Results Myocardial infarct size was significantly reduced in Group C(26.4%±1.83%) when compared with that of Group B(46.8%±1.41%),Group D(34.5%±1.56%) and Group E(31.5%±1.27%).Plasma TNF-α and IL-6 concentration in Group C were lower than those in Group B,Group D and Group E at 120mins of reperfusion,but higher than in Group A(P<0.01).Conclusion Butorphanol postconditioning has cardio-protective effects and can restrain the inflammatory factor releasing from injured hearts.The potential mechanism of this phenomenon might be associated with decreasing the injury by activating κ-opioid receptor,and avoiding calcium overload.