羟考酮用于缺血后处理对家兔心肌缺血再灌注损伤的影响

发布时间：2018-03-15 00:37

本文选题：羟考酮　切入点：再灌注损伤　出处：《山东医药》2017年06期 　论文类型：期刊论文

【摘要】：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(P0.05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。
[Abstract]:Objective to investigate the protective effect of hydroxycodone on myocardial ischemia and reperfusion in rabbits, and to observe the role of 魏 receptor in myocardial ischemia. Methods Forty-eight male rabbits were randomly divided into 4 groups. In the sham operation group, the left anterior descending branch was only threaded and not ligated, while in the ischemia reperfusion group, the left anterior descending branch was ligated for 30 minutes after thoracotomy, and the ischemia reperfusion model was established for 180 minutes after reperfusion. The hydroxycodone post-treatment group received hydroxycodone 0.3 mg / kg slowly 5 minutes before the beginning of reperfusion, while the 魏 receptor antagonist hydroxycodone treated group was given 魏 receptor antagonist 3 mg / kg 10 min before reperfusion, and the remaining treatment was treated with hydroxycodone post-treatment. Group 1. Serum CK-MBN cTnI levels were measured at the end of reperfusion. Myocardial infarction area was measured by TTC method, myocardial infarction area percentage was calculated and myocardial tissue was retained. Immunohistochemical staining method was used to detect the expression of gap junction protein 43 (CX43). The level of CK-MBN cTnI increased and the expression of CX43 decreased in both groups. Compared with the ischemia-reperfusion group, the level of IS/LVS in the treated group was lower than that in the control group, and the expression of CX43 in the treated group was significantly lower than that in the control group (P < 0.05), compared with that in the ischemia-reperfusion group. Serum CK-MBN cTn-I decreased the expression of CX43 increased (P0.05 or 0.01). Compared with hydroxycodone post-treated group, the level of IS/LVS and serum CK-MBcTn-I increased in the kappa receptor antagonist hydroxone posttreatment group. Conclusion the level of CX43 expression decreased in both groups. Conclusion Hydrocodone ischemic treatment can decrease the expression of CX43. Serum CK-MBN cTn-I, reducing IS, can reduce myocardial ischemia-reperfusion injury. The mechanism may be the regulation of CX43 expression after activation of 魏 receptor to play a role in myocardial protection.
【作者单位】：河北大学附属医院;河北大学;保定市第一医院;
【分类号】：R54

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