CAJ | 학술논문

目的：探讨NO/cGMP信号通路在鞘内吗啡预处理减轻大鼠心肌缺血/再灌注损伤中的作用。方法大鼠建立鞘内置管的模型。随机分为9组,每组6只：SHAM组(假手术组)、CON组(对照组,生理盐水)、ITMP组(鞘内吗啡预处理,3μg·kg-1)、L-NAME+ITMP组(一氧化氮合酶阻断剂+鞘内吗啡预处理)、ODQ+ITMP组(鸟苷酸环化酶阻断剂+鞘内吗啡预处理)、KT5823+ITMP组(蛋白激酶G阻断剂+鞘内吗啡预处理)、L-NAME组、ODQ 组、KT5823组。 IT-MP组于心脏缺血前,鞘内注射吗啡10μl 5 min,间断5 min,重复3次；CON组以相同的方式注射生理盐水；L-NAME+ITMP组、ODQ+ITMP组、KT5823+ITMP组分别于吗啡预处理前10 min 鞘内注射 L-NAME(30 nmol,10μl)、ODQ(11 nmol,10μl)、KT5823(20 pmol,10μl)；L-NAME组、ODQ组、KT5823组为阻断剂自身对照组。除SHAM组行假手术操作不做其他处理,其余各组大鼠均行左冠状动脉缺血30 min,再灌注120 min 诱导心肌缺血/再灌注损伤。观察指标包括：血流动力学指标；心肌缺血危险区( AAR )、梗死区( IS )的体积、心肌梗死面积以IS/AAR表示。结果与CON组相比,ITMP组的IS和IS/AAR均明显下降(P<0.01)；与ITMP组比较,L-NAME+ITMP组、ODQ+ITMP组、KT5823+ITMP组的IS和IS/AAR均升高( P<0.01)。与SHAM组比较各组MAP和 RPP在缺血30 min降低(P<0.05),与基础值比较,除SHAM组外,其余各组MAP和RPP在缺血30 min降低(P<0.05)。结论 NO/cGMP的信号通路可能参与介导鞘内吗啡预处理,对大鼠心肌缺血/再灌注损伤的保护作用。
목적：탐토NO/cGMP신호통로재초내마배예처리감경대서심기결혈/재관주손상중적작용。방법대서건립초내치관적모형。수궤분위9조,매조6지：SHAM조(가수술조)、CON조(대조조,생리염수)、ITMP조(초내마배예처리,3μg·kg-1)、L-NAME+ITMP조(일양화담합매조단제+초내마배예처리)、ODQ+ITMP조(조감산배화매조단제+초내마배예처리)、KT5823+ITMP조(단백격매G조단제+초내마배예처리)、L-NAME조、ODQ 조、KT5823조。 IT-MP조우심장결혈전,초내주사마배10μl 5 min,간단5 min,중복3차；CON조이상동적방식주사생리염수；L-NAME+ITMP조、ODQ+ITMP조、KT5823+ITMP조분별우마배예처리전10 min 초내주사 L-NAME(30 nmol,10μl)、ODQ(11 nmol,10μl)、KT5823(20 pmol,10μl)；L-NAME조、ODQ조、KT5823조위조단제자신대조조。제SHAM조행가수술조작불주기타처리,기여각조대서균행좌관상동맥결혈30 min,재관주120 min 유도심기결혈/재관주손상。관찰지표포괄：혈류동역학지표；심기결혈위험구( AAR )、경사구( IS )적체적、심기경사면적이IS/AAR표시。결과여CON조상비,ITMP조적IS화IS/AAR균명현하강(P<0.01)；여ITMP조비교,L-NAME+ITMP조、ODQ+ITMP조、KT5823+ITMP조적IS화IS/AAR균승고( P<0.01)。여SHAM조비교각조MAP화 RPP재결혈30 min강저(P<0.05),여기출치비교,제SHAM조외,기여각조MAP화RPP재결혈30 min강저(P<0.05)。결론 NO/cGMP적신호통로가능삼여개도초내마배예처리,대대서심기결혈/재관주손상적보호작용。
Aim To investigate the role of NO/cGMP in the cardioprotective effects of intrathecal morphine preconditioning against myocardial ischemia-reperfu-sion injury in rats. Method 54 Male Sprague-Dawley Rats were used to establish the model of intrathecal catheter placement. The rats were randomly assigned to <br> 9 groups. SHAM (sham group), CON (control, sa-line) , ITMP ( intrathecal morphine preconditioning, 3μg·kg-1 ) , L-NAME+ITMP ( NO synthetase inhibi-tor,L-NAME ) , ODQ + ITMP ( guanylate cyclase in-hibitor, ODQ ) , KT5823 + ITMP ( PKG inhibitor, KT5823),L-NAME,ODQ,KT5823,6ratsineach <br> group. ITMP were produced by three cycles of 5 min intrathecal injection of morphine and 5 min intermis-sion before myocardial ischemia, CON were achieved by intrathecal injection of saline in the same way, L-NAME+ITMP, ODQ +ITMP, KT5823 +ITMP were prepared by intrathecally administering L-NAME ( 30 nmol), ODQ(11 nmol) and KT5823(20 pmol) 10 minutes prior to ITMP respectively, L-NAME, ODQ, KT5823 worked as the control of inhibitors themselves respectively without ITMP. Subsequently, all rats were subjected to 30 min of left coronary artery occlusion followed by 2 h of reperfusion except the SHAM group. Myocardial infarct size, as a percentage of the AAR, <br> was determined by 2 , 3 , 5-triphenyltetrazolium stai-ning. Results Compared with CON, the volumes of IS and IS/AAR were reduced in ITMP ( P <0.01 );the protective effects of ITMP were abolished by pre-treatment with L-NAME, ODQ and KT5823 ( P <0.01 );Conclusions NO/cGMP might be involved in the cardioprotective effect of intrathecal morphine pre-conditioning against myocardial ischemia and reperfu-sion injury in rats.