CAJ | 학술논문

目的探讨吗啡预处理-后处理对大鼠离体心脏缺血再灌注损伤的影响.方法雄性SD大鼠,体重180～200 g,应用Langendorff体外灌流装置,采用全心停灌45 min、再灌注60 min的方法制备大鼠离体心脏缺血再灌注模型.取模型制备成功的心脏40个,随机分为5组(n=8):缺血再灌注组(IR组)、吗啡预处理组(M1组)、吗啡后处理组(M2组)、吗啡预处理-后处理组(M1+M2组)、5-羟葵酸(5-HD)混合吗啡后处理组(5-HD+M2组).M1组全心停灌前30 min灌注含3.0 μmol/L吗啡的K-H液20 min,随后灌注K-H液10 min.M2组再灌注即刻灌注含3.0 μmol/L吗啡的K-H液10 min,随后灌注正常K-H液50 min.5-HD+M1组再灌注即刻灌注含3.0 μmol/L吗啡+10-4nunol/L 5-HD的K-H液10 min,随后灌注正常K-H液50 min.于再灌注60 min时,测定心肌肌酸激酶(CK-MB)活性,计算心肌梗死区与缺血危险区的比值(IS/AAR).结果与IR组相比,其余各组IS/AAR减少,CK-MB活性降低(P<0.05);与M2组比较,5-HD+M2组CK-MB活性及IS/AAR升高(P<0.05);M1组、M2组和M1+M2组上述指标比较差异无统计学意义(P>0.05).结论吗啡预处理.后处理虽然可减轻大鼠离体心脏缺血冉灌注损伤,但是与单独应用时效果相似,其原因可能是两者单独应用减轻心脏缺血再灌注损伤的机制均与开放线粒体ATP敏感性钾通道有关.
목적 탐토마배예처리-후처리대대서리체심장결혈재관주손상적영향.방법 웅성SD대서,체중180～200 g,응용Langendorff체외관류장치,채용전심정관45 min、재관주60 min적방법제비대서리체심장결혈재관주모형.취모형제비성공적심장40개,수궤분위5조(n=8):결혈재관주조(IR조)、마배예처리조(M1조)、마배후처리조(M2조)、마배예처리-후처리조(M1+M2조)、5-간규산(5-HD)혼합마배후처리조(5-HD+M2조).M1조전심정관전30 min관주함3.0 μmol/L마배적K-H액20 min,수후관주K-H액10 min.M2조재관주즉각관주함3.0 μmol/L마배적K-H액10 min,수후관주정상K-H액50 min.5-HD+M1조재관주즉각관주함3.0 μmol/L마배+10-4nunol/L 5-HD적K-H액10 min,수후관주정상K-H액50 min.우재관주60 min시,측정심기기산격매(CK-MB)활성,계산심기경사구여결혈위험구적비치(IS/AAR).결과 여IR조상비,기여각조IS/AAR감소,CK-MB활성강저(P<0.05);여M2조비교,5-HD+M2조CK-MB활성급IS/AAR승고(P<0.05);M1조、M2조화M1+M2조상술지표비교차이무통계학의의(P>0.05).결론 마배예처리.후처리수연가감경대서리체심장결혈염관주손상,단시여단독응용시효과상사,기원인가능시량자단독응용감경심장결혈재관주손상적궤제균여개방선립체ATP민감성갑통도유관.
Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .