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目的探讨羟考酮用于缺血后处理对缺血再灌注家兔心肌的保护作用,并观察κ受体在羟考酮缺血后处理中的作用。方法将48只雄性家兔随机分为4组,假手术组开胸后左前降支只穿线,不结扎;缺血再灌注组开胸后左前降支结扎心肌缺血30 min,再灌注180 min,建立缺血再灌注模型;羟考酮后处理组于再灌注起始前5min开始缓慢静脉给予羟考酮0.3 mg/kg;κ受体拮抗剂+羟考酮后处理组于再灌注起始前10 min给予κ受体拮抗剂3 mg/kg,余处理同羟考酮后处理组。于再灌注末测定各组血清CK-MB、cTnI水平,TTC法测定心肌梗死面积(IS),计算心肌梗死面积百分比(IS/LVS)。留取心肌组织,免疫组化染色法检测细胞缝隙连接蛋白43(CX43)表达。结果与假手术组比较,缺血再灌注组、羟考酮后处理组、κ受体拮抗剂+羟考酮后处理组血清CK-MB、cTnI水平升高,CX43表达降低(P均<0.05)。与缺血再灌注组比较,羟考酮后处理组IS/LVS降低,血清CK-MB、cTn-I水平降低,CX43表达升高(P<0.05或<0.01)。与羟考酮后处理组比较,κ受体拮抗剂+羟考酮后处理组IS/LVS及血清CK-MB、cTn-I水平升高,CX43表达降低(P均<0.05)。结论羟考酮缺血后处理能够降低血清CK-MB、cTn-I,减少IS,具有减轻心肌缺血再灌注损伤的作用;其机制可能是通过激动κ受体后调节CX43表达来发挥心肌保护作用。
Objective To investigate the protective effect of oxycodone on ischemic postconditioning in rabbits with myocardial ischemia and reperfusion and to observe the role of κ receptor in the postconditioning of oxycodone ischemia. Methods Forty-eight male rabbits were randomly divided into four groups. Sham-operated group, the left anterior descending branch was only threaded and non-ligated. The left anterior descending branch of the ischemia-reperfusion group was ligated for 30 minutes and reperfused for 180 minutes , The model of ischemia-reperfusion was established. Oxycodone-treated group began slowly intravenous oxycodone 0.3 mg / kg 5 min before reperfusion, while the group of κ-receptor antagonist + oxycodone post-reperfusion Kappa receptor antagonist 3 mg / kg was given in the first 10 min, while the rest was treated with oxycodone. Serum levels of CK-MB and cTnI were measured at the end of reperfusion. The myocardial infarct size (IS) was measured by TTC method and the percentage of myocardial infarction area (IS / LVS) was calculated. Myocardial tissues were collected and the expression of connexin43 (CX43) was detected by immunohistochemistry. Results Compared with the sham-operation group, the levels of CK-MB and cTnI in the ischemic reperfusion group, the oxycodone post-treatment group and the kappa-receptor antagonist + oxycodone post-treatment group were significantly higher than those in the sham operation group (all P <0.05 ). Compared with the ischemia / reperfusion group, the levels of IS / LVS, CK-MB and cTn-I in the oxycodone-treated group decreased and the expression of CX43 increased (P <0.05 or <0.01). Compared with the oxycodone group, IS / LVS and CK-MB, cTn-I levels in the kappa receptor antagonist + oxycodone treatment group were significantly decreased and CX43 expression was decreased (all P <0.05). Conclusions Oxycodone ischemic postconditioning can reduce serum CK-MB and cTn-I, decrease IS, and reduce myocardial ischemia-reperfusion injury. The mechanism may be that myocardium protection is exerted by regulating the expression of CX43 after activation of κ receptor effect.