CAJ | 학술논문

目的:观察痛敏素/孤啡肽(N/OFQ)对脑缺血大鼠梗死体积和体感诱发电位(SEP)的影响.方法:41只SD大鼠随机分为大脑中动脉闭塞(MCAO)假手术组(n=5)、缺血组(n=8)、N/OFQ 10μg 组(n=7)、N/OFQ 1 μg组(n=7)、N/OFQ0.1μg组(n=7)和人工脑脊液(ACSF)组(n=7).采用腔内线栓法制作大鼠MCAO模型,MCAO后2 h再灌注.N/OFQ 10μg组、N/OFQ μg组、N/OFQ0.1μg组和ACSF组分别在MCAO后1 h脑室内注射N/OFQ 10μg、N/OFQ 1μg、N/OFQ0.1 μg和体积相同ACSF.检测再灌注24 h后脑梗死体积体,并记录SEP.结果:假手术组SEP PI波幅降低,P1峰潜时间无显著变化.N/OFQ 0.1 μg组SEP波幅、P1峰潜时间和脑梗死体积与ACSF组无显著差异.N/OFQ μg组和N/OFQ10 μg组SEP波幅较ACSF组进一步降低,但P1峰潜时间无显著变化.ACSF组SEP波幅在再灌注后1 h基本恢复至缺血前水平,N/OFQ 1 μg组恢复减慢,N/OFQ10 μg组直到再灌注后3 h仍未恢复.N/OFQ剂量与SEP反应呈量效关系,剂量越大,SEP抑制越显著,恢复越慢.再灌注24 h时,假手术组、ACSF组、N/OFQ0.1 μg组、N/OFQ1 μg组和N/OFQ 10 μg组脑梗死体积分别为0 mm3、(24.180±4.088)mm3、(23.090±4.523)mm3、(35.304±6.824)mm3和(40.806±6.716)mm0.N/OFQ 0.1μg组与ACSF组无显著差异,N/OFQ μg组和N/OFQ 10 μg组与ACSF组均有显著差异(P均＜0.01).结论:脑缺血早期侧脑室注射N/OFQ町使SEP波幅降低、恢复时间延长,梗死体积增大,表明其可加重缺血性脑损伤.
목적:관찰통민소/고배태(N/OFQ)대뇌결혈대서경사체적화체감유발전위(SEP)적영향.방법:41지SD대서수궤분위대뇌중동맥폐새(MCAO)가수술조(n=5)、결혈조(n=8)、N/OFQ 10μg 조(n=7)、N/OFQ 1 μg조(n=7)、N/OFQ0.1μg조(n=7)화인공뇌척액(ACSF)조(n=7).채용강내선전법제작대서MCAO모형,MCAO후2 h재관주.N/OFQ 10μg조、N/OFQ μg조、N/OFQ0.1μg조화ACSF조분별재MCAO후1 h뇌실내주사N/OFQ 10μg、N/OFQ 1μg、N/OFQ0.1 μg화체적상동ACSF.검측재관주24 h후뇌경사체적체,병기록SEP.결과:가수술조SEP PI파폭강저,P1봉잠시간무현저변화.N/OFQ 0.1 μg조SEP파폭、P1봉잠시간화뇌경사체적여ACSF조무현저차이.N/OFQ μg조화N/OFQ10 μg조SEP파폭교ACSF조진일보강저,단P1봉잠시간무현저변화.ACSF조SEP파폭재재관주후1 h기본회복지결혈전수평,N/OFQ 1 μg조회복감만,N/OFQ10 μg조직도재관주후3 h잉미회복.N/OFQ제량여SEP반응정량효관계,제량월대,SEP억제월현저,회복월만.재관주24 h시,가수술조、ACSF조、N/OFQ0.1 μg조、N/OFQ1 μg조화N/OFQ 10 μg조뇌경사체적분별위0 mm3、(24.180±4.088)mm3、(23.090±4.523)mm3、(35.304±6.824)mm3화(40.806±6.716)mm0.N/OFQ 0.1μg조여ACSF조무현저차이,N/OFQ μg조화N/OFQ 10 μg조여ACSF조균유현저차이(P균＜0.01).결론:뇌결혈조기측뇌실주사N/OFQ정사SEP파폭강저、회복시간연장,경사체적증대,표명기가가중결혈성뇌손상.
Oyecave:To observe the influence of nociceptin/orphanin FQ(N/OFO)on cerebral infarction volume and somatosellsOry evoked potential(SEP)in focal cerebral ischemia in rats.Methods:Forty one SD rats were randomly alloomed into middle artery occlusion(MCAO)sham-operation(n=5),isehemic(n=8),N/OFQ 10μg(n=7),N/OFQ 1 μg(n=7),N/OFQ0.1 μg(n=7),and artificiai cerebrospinal fluid(ACSF)(n=7)groups.A model of middle cerebral artery occlusion(MCAO)in rats was induced using intraluminal suture method.Reperfusion was performed 2 hours after MCAO.One hour after MCAO,N/OFQ 10 μg,N/OFQ 1 μg,N/OFQ O. 1 μg,and the same volume of ACSF were injected intraventricularly in the N/OFQ 10 μg,N/OFQ 1 μg,N/OFQ 0. 1 μg,and ACSF groups,respectively. The cerebral infarction volurne was detected 24 hours after reperfusion,and SEP was recorded. Results:1he amplitude of SEP P1 decreased in the sham-operation group. There was no significant change in P1 peak latencies.There were no significant differences hetween the N/OFQ 0. 1 μg group and the ACSF group in SEP amplitudes,P1 peak lantecies and cerebral infarction volume. As compared with the ACSF group,the SEP amplitudes were further decreased in the N/OFQ 1 μg and N/OFQ 10 μg groups,but there were no significant change in P1 peak lantecies. One hour after reperfusion,the SEP amplitude in the ACSF group almost returned to the level of preischemia,the recovery slowed down in the N/OFQ 1 μg group,and it still did not recovered 3 hours after reperfusion in the N/OFQ 10 μg group. The dose of N/OFQ and SEP response showed dose-effect relationship,The higher the dose,the deeper the SEP depression and the slower the recovery. At 24 hours after reperfusion,the cerebral infarction vlumes in the shamoperation,ACSF,N/OFQ 0. 1 μg,N/OFQ 1 μg,and N/OFQ 10 μg groups were 0 mm3,24.180 ±4.088 mm3,23.090±4.523 mm3,35.304 ± 6. 824 mm3,and 40. 806±6. 716 mm3,respectively. There was no significant difference between N/OFQ 0. 1 and ACSF groups. There were significant differences between N/OFQ 1 μg and 10 μg groups and ACSF group (all P ＜ 0.01 ). Conclusions:Intracerebroventricular injection of N/OFQ in the early stage of cerebral ischemia decreases the SEP amplitude,prolongs the time of recovery,and increases cerebral infarction volume,which shoves that it may aggravate cerebral ischemic injury.