布托啡诺后处理对大鼠心肌缺血再灌注损伤的影响

目的:探讨布托啡诺后处理是否具有减轻心肌缺血再灌注损伤的作用及其可能的机制.方法:通过结扎冠状动脉前降支30 min、开放120 min的方法建立心肌缺血再灌注模型.健康SPF‘级成年雄性Wistar大鼠10只,随机分为5组(各组分别10只).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...

Effect of Butorphanol Postconditioning on Myocardial Ischemia Reperfusion Injury in Rats

Objective: To explore the effects of postconditioning of butorphanol on ischemia reperfusion (I/R) injury in rats and the potential mechanism. Methods: The rat model of ischemia reperfusion was established by the ligation of left anterior coronary descending branch (LAD) for 30 min and removing the ligation for 120 min. Fifty anesthetized adult male rats were randomly divided into five groups as group A-E according to the treatment of sham operation, I/R, I/R + butorphanol postconditioning, I/R + butorphanol + Nor-BNI, and I/R + butorphanol + glibenclamide respectively, and each group had 10 rats. The myocardial infarct size was examined by weighing after using TTC staining. And the myocardial tissue superoxide dismutase (SOD), malondialdehyde (MDA) activity and myeloperoxidase (MPO) were determined. Results: Myocardial infarct size was significantly reduced in group C (26.4%±1.83%) as compared with that of group B (46.8%±1.41%), group D (34.5%±1.56%), and group E (31.5%±1.27%) respectively. While the MDA and MPO activity of ischemic area in group C were significantly less than those in group B, D, and E (all P<0.01) respectively. The SOD activity in group C was higher than that in all the other groups (all P<0.01). Conclusion: As to ischemic myocardium, postconditioning of butorphanol tartrate could provide potent myocardial infarct size reduction and cardio-protective effect. The potential mechanism might be associated with decreasing the injury by activating kappa-opioid receptor, opening the mitochondrial K(ATP) channels, avoiding calcium overload and decreasing peroxidation.