CAJ | 학술논문

目的探讨不同剂量纳洛酮后处理对大鼠局灶性脑缺血再灌注损伤的影响.方法成年sD大鼠88只,体重270～330 g,随机分为4组(n=22):假手术组(S组)、脑缺血再灌注组(IR组)和不同剂量纳洛酮后处理组(N_(1,2)组).除S组外,其它3组均采用阻断右侧大脑中动脉90 min、再灌注24 h的方法制备局灶性脑缺血再灌注损伤模型.N_(1,2)组于再灌注即刻分别腹腔注射纳洛酮1、10 mg/kg,S组和m组给予等容量生理盐水.分别于再灌注2、24 h时测定大鼠神经功能障碍评分(NDS);再灌注24 h时测定脑梗死面积和脑组织微管相关蛋白2(MAP2)的表达水平和脑组织血浆容量、徽血管直径和长度.结果与S组相比,IR组、N_(1,2)组NDS评分均升高,脑梗死面积增大,脑组织MAP2表达水平下调,缺血侧脑组织血浆容量降低,微血管直径和长度减小(P<0.05);与IR组相比,N_2组NDS评分降低,脑梗死面积减小,脑组织MAP2表达水平上调,缺血侧脑组织血浆容量升高,微血管直径和长度增大(P<0.05),N_1组上述指标差异无统计学意义(P>0.05);与N_1组相比,N_2组NDS评分降低,脑梗死面积减小,脑组织MAP2表达水平上调,缺血侧脑组织血浆容量升高,微血管直径和长度增大(P<0.05).结论纳洛酮后处理可减轻大鼠局灶性脑缺血再灌注损伤,且呈剂量依赖性.
목적 탐토불동제량납락동후처리대대서국조성뇌결혈재관주손상적영향.방법 성년sD대서88지,체중270～330 g,수궤분위4조(n=22):가수술조(S조)、뇌결혈재관주조(IR조)화불동제량납락동후처리조(N_(1,2)조).제S조외,기타3조균채용조단우측대뇌중동맥90 min、재관주24 h적방법제비국조성뇌결혈재관주손상모형.N_(1,2)조우재관주즉각분별복강주사납락동1、10 mg/kg,S조화m조급여등용량생리염수.분별우재관주2、24 h시측정대서신경공능장애평분(NDS);재관주24 h시측정뇌경사면적화뇌조직미관상관단백2(MAP2)적표체수평화뇌조직혈장용량、휘혈관직경화장도.결과 여S조상비,IR조、N_(1,2)조NDS평분균승고,뇌경사면적증대,뇌조직MAP2표체수평하조,결혈측뇌조직혈장용량강저,미혈관직경화장도감소(P<0.05);여IR조상비,N_2조NDS평분강저,뇌경사면적감소,뇌조직MAP2표체수평상조,결혈측뇌조직혈장용량승고,미혈관직경화장도증대(P<0.05),N_1조상술지표차이무통계학의의(P>0.05);여N_1조상비,N_2조NDS평분강저,뇌경사면적감소,뇌조직MAP2표체수평상조,결혈측뇌조직혈장용량승고,미혈관직경화장도증대(P<0.05).결론 납락동후처리가감경대서국조성뇌결혈재관주손상,차정제량의뢰성.
Objective To investigate whether naloxone postconditioning could attenuate the focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Eighty-eight adult male SD nits weighing 270-330 g were randomly divided into 4 groups (n = 22 each) : group I sham operation (S); group Ⅱ I/R; group Ⅲ , Ⅳ I/R + low and high dose naloxone ( N_1, N_2). Focal cerebral I/R was produced by occlusion of right middle cerebral artery for 90 min followed by 24 h reperfusion. In group N_1, and N_2 naloxone 1 and 10 mg/kg were injected intraperitoneally at initiation of reperfusion respectively. In group I/R normal saline was injected instead of naloxone. HR, MAP and EKG were continuously monitored throughout the experiment. He neurological deficits were scored (0 = no deficit, 4 = unable to crawl, mental dysfunction) at 2 h and 24 h of reperfusion. The animals were then decapitated. The brains were immediately removed for determination of infarct size ( n = 10) and the expression of microtubule-associated protein-2 ( MAP-2) in brain tissue ( n = 6) . In the other 6 rats in each group FICT-dextran 1 ml (50 mg/ml) was injected iv at 1 min before decapitation. The cerebral plasma volume and diameter and segment length of cerebral microvessels on the I/R side were measured using laser scanning confocal microscopy (LSCM). Results Focal cerebral I/R significantly increased neurological deficit scores, induced cerebral infarct, and decreased MAP-2 expression in the brain tissue, cerebral plasma volume and the diameter and segment length of cerebral microvessels on the I/R side. Postconditioning with 10 mg/kg naloxone significantly attenuated the above-mentioned focal cerebral I/R-induced changes. Conclusion Postconditioning with naloxone can attenuate focal cerebral I/R injury in a dose-dependent manner.