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作 者:唐昱英[1] 林严俊[2] 李吉满[3] 万俊峰[3] 黄蔚[1]
机构地区:[1]四川大学华西第二医院麻醉科,成都市610041 [2]四川大学华西医院麻醉科 [3]四川省肿瘤医院病理科
出 处:《中华麻醉学杂志》2011年第3期350-353,共4页Chinese Journal of Anesthesiology
基 金:四川省科技厅科技支撑计划项目(2010SZ0185)
摘 要:目的探讨低温人工脑脊液灌流对兔脊髓缺血再灌注时水通道蛋白.4(AQP-4)表达的影响。方法成年雄性新西兰大白兔54只,采用随机数字表法,将其随机分为3组(n=18):假手术组(S组)、脊髓缺血再灌注组(I/R组)和低温人工脑脊液灌流组(FI组)。I/R组和FI组采用阻断肾下腹主动脉60min后开放的方法制备脊髓缺血再灌注模型。FI组阻断腹主动脉时以30ml/h的速率经L4.,间隙蛛网膜下腔输注25℃人工脑脊液,同时开放L7,8间隙蛛网膜下腔引流脑脊液。腹主动脉开放的同时停止人工脑脊液灌流。每组取6只动物,分别在再灌注4、24、48、72h时进行神经功能评分;每组分别于再灌注4、24、72h时取6只动物,取L5-8脊髓节段,计算脊髓组织含水量,并测定AQP-4表达水平。结果与S组比较,I/R组神经功能评分降低,脊髓组织含水量增加,AQP-4表达下调(P〈0.05)。与I/R组比较,FI组神经功能评分升高,脊髓组织含水量降低,AQP-4表达上调(P〈0.05)。结论低温人工脑脊液灌流可上调AQP-4表达,从而减轻兔脊髓缺血再灌注损伤。Objective To investigate the effect of irrigation with hypothermic artificial cerebral-spinal fluid (aCSF) on expression of aquaporin-4 (AQP-4) in the spinal cord following spinal ischemia-reperfusion (I/R) in rabbits. Methods Fifty-four adult male New Zealand white rabbits weighing 2.0-2.5 kg were randomly divided into 3 groups (n = 18 each): group sham operation (S group); group I/R and group irrigation with hypothermic aCSF (FI group). Spinal I/R was induced by clamping the abdominal aorta below renal artery for 60 min. Hypot- hermic aCSF (25 ℃ ) was infused at L4,s interspace at a rate of 30 ml/h and drained from L7,8 interspace during spinal ischemia. Neurological function was evaluated at 4, 24, 48 and 72 h of reperfusion and scored (0 = no hind limb activity, 4 = hind limb function completely recovered) in 6 animals in each group. Six animals were sacrificed at 4, 24 and 72 h respectively in each group. The lumbar segment ( L5-8 ) was removed for measurement of water content and AQP-4 protein expression (by immuno-histochemistry). Results Neurological function scores were significantly lower, water content was higher and AQP-4 expression smaller in group I/R than in group S. I/R-in- duced effects were significantly attenuated by irrigation of hypothermic aCSF. Conclusion Irrigation with hypothermic aCSF can ameliorate the spinal cord I/R injuries by up-regulation of AQP-4 expression.
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