CAJ | 학술논문

目的探讨不同阿片受体在舒芬太尼后处理减轻大鼠心肌缺血再灌注损伤中的作用.方法健康雄性SD大鼠50只,4～6月龄,体重200 ～ 330 g,采用随机数字表法,将其分为9组,缺血再灌注组(I/R组,n=7)采用结扎左冠状动脉前降支(LAD)30 min、再灌注120 min的方法制备大鼠心肌缺血再灌注损伤模型；缺血后处理组(IPC组,n=7)再灌注前行缺血后处理,进行3个循环的10 s开放LAD 10 s阻断LAD；舒芬太尼后处理组(SP组,n=6)于再灌注前5 min静脉注射舒芬太尼1μg/kg行舒芬太尼后处理；κ受体拮抗剂nor-binaltorphimne+舒芬太尼后处理组(BNI+ SP组,n=5)、δ受体拮抗剂纳曲吲哚+舒芬太尼后处理组(NTD+ SP组,n=5)和μ受体拮抗剂CTOP+舒芬太尼后处理组(CTOP+ SP组,n=5)于舒芬太尼后处理前分别静脉注射BNI 5 mg/kg、纳曲吲哚5 mg/kg和CTOP 1 mg/kg;BNI组、NTD组和CTOP组分别于再灌注前5 min时静脉注射相应剂量BNI、纳曲吲哚和CTOP.于再灌注120 min时采集颈总动脉血样,测定血浆cTnI浓度,处死大鼠后,取心脏,确定心肌梗死(IS)与缺血危险区(AAR)体积的比值(IS/AAR值).结果与I/R组比较,IPC组、SP组、BNI+ SP组和NTD+ SP组血浆cTnI浓度和IS/AAR值降低(P＜0.05),CTOP+ SP组、NTD组、BNI组和CTOP组血浆cTnI浓度和IS/AAR值差异无统计学意义(P＞0.05)；与SP组比较,BNI+ SP组和NTD+ SP组IS/AAR值升高,CTOP+ SP组血浆cTnI浓度和IS/AAR值升高(P＜0.05).结论 μκ和δ阿片受体均介导了舒芬太尼后处理减轻大鼠心肌缺血再灌注损伤.
목적 탐토불동아편수체재서분태니후처리감경대서심기결혈재관주손상중적작용.방법 건강웅성SD대서50지,4～6월령,체중200 ～ 330 g,채용수궤수자표법,장기분위9조,결혈재관주조(I/R조,n=7)채용결찰좌관상동맥전강지(LAD)30 min、재관주120 min적방법제비대서심기결혈재관주손상모형；결혈후처리조(IPC조,n=7)재관주전행결혈후처리,진행3개순배적10 s개방LAD 10 s조단LAD；서분태니후처리조(SP조,n=6)우재관주전5 min정맥주사서분태니1μg/kg행서분태니후처리；κ수체길항제nor-binaltorphimne+서분태니후처리조(BNI+ SP조,n=5)、δ수체길항제납곡신타+서분태니후처리조(NTD+ SP조,n=5)화μ수체길항제CTOP+서분태니후처리조(CTOP+ SP조,n=5)우서분태니후처리전분별정맥주사BNI 5 mg/kg、납곡신타5 mg/kg화CTOP 1 mg/kg;BNI조、NTD조화CTOP조분별우재관주전5 min시정맥주사상응제량BNI、납곡신타화CTOP.우재관주120 min시채집경총동맥혈양,측정혈장cTnI농도,처사대서후,취심장,학정심기경사(IS)여결혈위험구(AAR)체적적비치(IS/AAR치).결과 여I/R조비교,IPC조、SP조、BNI+ SP조화NTD+ SP조혈장cTnI농도화IS/AAR치강저(P＜0.05),CTOP+ SP조、NTD조、BNI조화CTOP조혈장cTnI농도화IS/AAR치차이무통계학의의(P＞0.05)；여SP조비교,BNI+ SP조화NTD+ SP조IS/AAR치승고,CTOP+ SP조혈장cTnI농도화IS/AAR치승고(P＜0.05).결론 μκ화δ아편수체균개도료서분태니후처리감경대서심기결혈재관주손상.
Objective To evaluate the role of different opioid receptors in sufentanil postconditioning-induced attenuation of myocardial ischemia-reperfusion (I/R) injury in rats.Methods Fifty adult male Sprague-Dawley rats,aged 4-6 months,weighing 200-330 g,were randomly divided into 9 groups:I/R group (n =7),ischemic postconditioning (IPC) group (n =7),sufentanil postconditiong (SP) group (n =6),κ-opioid receptor antagonist nor-binaltorphimine (nor-BNI) + SP group (group BNI + SP,n =5),δ-opioid receptor antagonist naltrindole + SP group (group NTD + SP,n =5) and μ-opioid receptor antagonist CTOP + SP group (group CTOP +SP,n =5).Myocardial I/R was produced by 30 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion.IPC was induced by 3 episodes of 10 s reperfusion followed by 10 s ischemia at the end of 30 min myocardial ischemia.Sufentanil 1 μg/kg was injected intravenously at 5 min before reperfusion in SP group.In groups BNI + SP,NTD + SP and CTOP + SP,nor-BNI 5 mg/kg,naltrindole 5 mg/kg and CTOP 1 mg/kg were injected intravenously,respectively,before SP and the corresponding doses of nor-BNI,naltrindole and CTOP were injected intravenously,respectively,at 5 min before reperfusion.Arterial blood samples were collected at 120 min of reperfusion for measurement of the plasma cardiac tropnin I (cTnI) concentration.The rats were then sacrificed and hearts removed for determination of myocardial infarct size (IS) and area at risk (AAR).IS/AAR was calculated.Results Compared with I/R group,the plasma cTnI concentration and IS/AAR were significantly decreased in groups IPC,SP,BNI + SP and NTD + SP (P ＜ 0.05),and no significant change was found in the plasma cTnI concentration and IS/AAR in groups CTOP + SP,NTD,BNI and CTOP (P ＞ 0.05).Compared with SP group,IS/AAR was increased in NTD + SP and BNI + SP groups and the plasma cTnI concentration and IS/AAR were significantly increased in CTOP + SP group (P ＜ 0.05).Conclusion The μ-,κ-and δ-opioid receptors mediate sufentanil postconditioning-induced attenuation of myocardial I/R injury in rats.