【摘要】：目的:既往研究結(jié)果顯示缺血后處理(Iscemia Postconditioning)能夠減輕心肌缺血再灌注損傷。本實驗旨在探明鹽酸羥考酮注射液(Oxycodone Hydrochloride Injection)用于后處理是否產(chǎn)生上述保護效應(yīng),以及了解κ受體在羥考酮后處理中的作用。方法:健康雄性家兔,2~3月齡,體重2.2~2.8 k g,建立心肌缺血再灌注損傷模型,家兔開胸后左前降支給予30min結(jié)扎和180min再灌注,隨機分為5組:1)假手術(shù)組(sham組,n=8)左前降支只穿線,不結(jié)扎;2)缺血再灌注組(I/R組,n=9):左前降支結(jié)扎心肌缺血30 min,再灌注180 min;3)缺血后處理組(Ipoc組,n=9):再灌注起始3min內(nèi)給予重復(fù)3次的30s缺血/30s再灌;4)羥考酮后處理組(Oxpoc組,n=9):再灌注起始前5min開始緩慢靜脈給予羥考酮(0.3mg/kg);5)nor-binaltorphimne+羥考酮后處理組(BNI+Oxpoc組,n=10):再灌注起始前10min給予κ受體拮抗劑nor-binaltorphimne(3mg/kg),余處理同Oxpoc組。再灌注末測定血清cTnI濃度、TTC法測定心肌梗死面積,計算心肌梗死面積百分比(IS/LV)。留取心肌組織,免疫組化染色法檢測細胞縫隙連接蛋白43(CX43蛋白)的表達,計算其平均光密度OD值。結(jié)果:與Sham組比較,其余四組血清CK-MB、cTn-I濃度升高(P0.05),Cx43OD值降低(P0.05);與I/R組比較,Ipoc組、Oxpoc組心肌梗死面積百分比、血清CK-MB、cTnI濃度降低(P0.05),Ipoc組、Oxpoc組Cx43 OD值升高(P0.05);與Ipoc組或Oxpoc組比較,BNI+Oxpoc組心肌梗死面積百分比和血清CK-MB、cTnI濃度升高(P0.05),Cx43 OD值降低(P0.05)。結(jié)論:1.羥考酮后處理具有與缺血后處理同等程度的減輕心肌缺血再灌注損傷作用。2.羥考酮后處理心肌保護作用的機制與κ受體的激活有關(guān)。3.羥考酮后處理可能通過激動κ阿片受體改善Cx43的表達與分布發(fā)揮心肌保護作用。
[Abstract]:Objective: previous studies have shown that post-ischemic (Iscemia Postconditioning) can reduce myocardial ischemia-reperfusion injury. The purpose of this study was to investigate the protective effect of hydroxycodone hydrochloride injection (Oxycodone Hydrochloride Injection) and the role of 魏 receptor in hydroxycodone aftertreatment. Methods: the model of myocardial ischemia reperfusion injury was established in healthy male rabbits, aged 2 to 3 months and weighing 2.2 ~ 2.8 kg. The left anterior descending branch was ligated with 30min and 180min reperfusion. The rabbits were randomly divided into 5 groups: 1) sham-operation group (sham group); The left anterior descending branch was only threaded and not ligated; 2) Ischemia-reperfusion group (I / R group, n / 9): left anterior descending branch ligated myocardial ischemia for 30 min, and reperfusion for 180 min;3) Ipoc group (n = 9): repeated 30 s ischemia / 30 s reperfusion in the initial 3min of reperfusion; 4) hydroxycodone post-treatment group (Oxpoc group, n = 9): 5min was given 0.3mg/kg slowly before reperfusion. 5) (BNI Oxpoc group (n = 10): 10min was given 魏 receptor antagonist nor-binaltorphimne (3mg/kg) before reperfusion, and the rest was treated with Oxpoc group. Serum cTnI concentration was measured at the end of reperfusion, myocardial infarction area was measured by TTC method and myocardial infarction area percentage (IS/LV) was calculated. The expression of gap junction protein 43 (CX43 protein) was detected by immunohistochemical staining and the mean optical density (OD) was calculated. Results: compared with the Sham group, the serum CK-MB,cTn-I concentration in the other four groups increased (P0.05) and the Cx43OD value decreased (P0.05). Compared with I / R group, the percentage of myocardial infarction size and serum CK-MB,cTnI concentration in Ipoc group and Oxpoc group decreased (P0.05), Ipoc group, Oxpoc group increased Cx43 OD value (P0.05); Compared with Ipoc group or Oxpoc group, the percentage of myocardial infarction area and serum CK-MB,cTnI concentration in, BNI Oxpoc group increased (P0.05), Cx43 OD value decreased (P0.05). Conclusion: 1. Hydroxycodone post-treatment has the same effect of alleviating myocardial ischemia-reperfusion injury as after-ischemia treatment. 2. 2. The mechanism of myocardial protection induced by hydroxycodone is related to the activation of 魏 receptor. 3. 3. Hydroxycodone postconditioning may improve the expression and distribution of Cx43 through activation of 魏 opioid receptor.
【學(xué)位授予單位】：河北大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R542.22

【參考文獻】

相關(guān)期刊論文 前9條

1 高潤霖;;冠心病疾病負擔(dān)—中國出路[J];中國循環(huán)雜志;2017年01期

2 侯軼楠;米衛(wèi)東;;鹽酸羥考酮的藥理作用及其在臨床上的應(yīng)用[J];感染、炎癥、修復(fù);2016年04期

3 楊s钅，

本文編號：2377473