低温对脑缺血/再灌注期间沙土鼠海马CA1区延迟性神经元死亡及ATP水平和细胞色素氧化酶活性的影响  

Effect of hypothermia on delayed neuronal death in hippocampal CA1 sector and ATP and cytochrome oxidase activity during cerebral ischemia/reperfusion in gerbils

作　　者：顾卫东[1] 陈群[2] 曾因明[3] 

机构地区：[1]上海瑞金医院集团闵行医院麻醉科,上海201100 [2]华盛顿天主教大学医学院内科,美国俄亥俄州克里夫兰市44106 [3]江苏省麻醉学重点实验室,江苏徐州221002

出　　处：《徐州医学院学报》2009年第1期4-7,共4页Acta Academiae Medicinae Xuzhou

摘　　要：目的观察低温对脑缺血/再灌注期间海马ATP水平和细胞色素氧化酶(CCO)活性的影响,以探讨低温减少延迟性神经元死亡(DND)的机制。方法采用沙土鼠前脑缺血/再灌注模型,缺血时间10 min。动物随机分为假手术组、常温组和低温组,3组动物又根据再灌注时间不同进一步分为再灌注6 h、48 h、96 h 3个亚组。所有沙土鼠脑缺血期间脑温均维持(38.0±0.2)℃,再灌注6 h内,低温组脑温维持(30.0±0.2)℃,常温组脑温维持(38.0±0.2)℃。光镜下观察海马CA1区存活锥体细胞数目。ATP、ADP、AMP含量测定采用高效液相紫外检测器法,CCO活性测定采用酶组织化学染色结合计算机图像分析。结果再灌注96 h,低温组海马CA1区存活锥体细胞数目明显多于常温组(P<0.01)。除再灌注6 h外,低温组海马ATP和腺苷酸池(ATP+ADP+AMP)含量均明显高于常温组(P<0.05)。低温组各再灌注时间点海马CA1区CCO活性均明显高于常温组(P<0.05)。结论低温可通过保护CCO活性减轻脑缺血/再灌注期间的细胞能量代谢障碍,从而减少DND。Objective To explore the mechanism of hypothermia reducing delayed neuronal death （DND） and the effect of hypothermia on ATP and cytochrome oxidase （CCO） activity during cerebral ischemia/reperfusion. Methods Forebrain ischemia/reperfusion model in gerbils was established by occlusion of bilateral common carotid arteries for 10 min. Gerbils were randomly divided into sham group, normothermia group and hypothermia group. These 3 groups were further divided into 3 subgroups according to the reperfusion time （6 h, 48 h, and 96 h）. The brain temperature in all gerbils during cerebral isehemia was kept at （38.0 ± 0.2 ） ℃. Within 6 h of reperfusion, the brain temperature was kept at （38.0 ±0. 2 ）℃ in normothermia group and at （30.0±0.2） ℃ in hypothermia group, respectively. The number of surviving neurons in hippoeampal CA1 sector was observed under light microscope. ATP, ADP and AMP were determined by high liquid chromatography. CCO activity was determined by enzyme histiochemieal staining and computer image system. Results The number of surviving neurons in hippocampal CA1 sector in hypothermia group was much higher than that in normothermia group after reperfusion of 96 h （ P 〈 0.01 ）. The level of ATP and adenine nucleotide pool in hippocampus in hypothermia group were much higher than that in normothermia group after reperfusion of 48 h and 96 h （ P 〈 0.05 ）. CCO activity in hypothermia group was much higher than that in normothermia group at all reperfusion time （ P 〈 0.01 ）. Conclusions Hypothermia attenuates the failure of energy metabolism by protecting CCO activity during cerebral ischemia/reperfusion, As a result, DND can be reduced.

关 键 词：缺血/再灌注损伤 脑 延迟性神经元死亡 细胞能量代谢 细胞色素氧化酶 沙土鼠 

分 类 号：R282.71[医药卫生—中药学] Q593.2[医药卫生—中医学]