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短暂异氟醚预处理诱导急性脑缺血耐受的时间效应
引用本文:郑玉,熊利泽,张西京,路志红,朱正华,刘艳红.短暂异氟醚预处理诱导急性脑缺血耐受的时间效应[J].临床麻醉学杂志,2004,20(8):503-505.
作者姓名:郑玉  熊利泽  张西京  路志红  朱正华  刘艳红
作者单位:710032,西安第四军医大学西京医院麻醉科
基金项目:国家自然科学基金课题 (基金号 :3 0 170 90 7)
摘    要:目的 观察异氟醚预处理诱导急性脑缺血耐受的时间效应。方法  4 0只雄性SD大鼠 ,随机分为四组 (每组 10只 ) :吸氧对照组 ,动物吸 10 0 %氧气 1h ;异氟醚预处理 1、2、3组 (Iso1组、Iso2组、Iso3组 ) ,动物接受 1h的异氟醚预处理 (1 5 %异氟醚 ,98 5 %氧气 )。在对照组吸氧 1h后 ,异氟醚预处理后 1、2、3h ,用右侧颈内动脉尼龙线线栓法致大脑中动脉阻闭 12 0min ,拔出尼龙线为再灌注时间。观察再灌注后 2 4h时神经功能损害改变并评分 ,2 4h时处死动物 ,取大脑行TTC染色以测量脑梗死容积。结果 术后动物均存活。缺血 再灌注后动物均表现一定神经功能障碍 ,再灌注2 4h内对照组神经功能障碍逐渐加重 ,各处理组则呈减轻趋势 ;再灌注 2 4h时神经功能损害评分(NDS)Iso1组和Iso2组明显低于对照组 (P <0 0 5 ) ;Iso3组与对照组间无显著性差异 ;Iso1组和Iso2组间NDS无显著性差异。再灌注 2 4h时脑梗死容积 ,Iso1组和Iso2组明显小于对照组 (P <0 0 5 ) ;Iso3组与对照组间及Iso1组与Iso2组间无显著性差异。结论  1h异氟醚预处理可诱导急性脑缺血耐受 ,其作用时间在预处理后 2h内。

关 键 词:异氟醚  预处理  急性脑缺血  耐受  时间效应
修稿时间:2003年9月24日

A study on the time course of acute ischemic tolerance of the brain induced by brief isoflurane inhalation
Zheng Yu,Xiong Lize,Zhang Xijing,et al..A study on the time course of acute ischemic tolerance of the brain induced by brief isoflurane inhalation[J].The Journal of Clinical Anesthesiology,2004,20(8):503-505.
Authors:Zheng Yu  Xiong Lize  Zhang Xijing  
Institution:Zheng Yu,Xiong Lize,Zhang Xijing,et al. Department of Anesthesiology,Xijing Hospital,The Fourth Military Medical University,Xi'an 710032 CHINA
Abstract:Objective To investigate the time course of acute ischemic tolerance of the brain induced by brief isoflurane anesthesia.Methods Forty male SD rats were randomly assigned to four groups (n=10 each): Animals in group control received 100% O 2 for 1 h, while the animals in Iso1, Iso2 and Iso3 groups received 1.5% isoflurane anesthesia in O 2 for 1 h. At 1 h after the pretreatment in group control and Iso1, and at 2 h and 3 h after the pretreatment in group Iso2 and Iso3 respectively, transient middle cerebral artery occlusion (MCAO) (120 min) was induced. The neurologic outcome was evaluated at 24 h after reperfusion. The brain infarct volume was then assessed by 2%TTC staining. Results The neurologic deficit scores (NDS) in groups Iso1 and Iso2 at 24 h after reperfusion were significantly lower than those in group control and Iso3 (P<0.05). The infarct volumes of group control and Iso3 were significantly larger than those of group Iso1 and Iso2(P<0.05) at 24h after reperfusion. There was no difference between group Iso1 and Iso2. Conclusion Brief isoflurane inhalation induces neuroprotective effect against transient focal cerebral ischemia within 2 h after pretreatment.
Keywords:Isoflurane  Preconditioning  Cerebral ischemic
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