依达拉奉对心肺复苏后大鼠脑神经细胞的保护作用  

The protective effect of Edaravone on apoptosis of cerebral neuron after cardiopulmonary resuscitation in rats

作　　者：周亚东[1] 杨琳[1] 史继学[1] 赵爱华[1] 姚静[1] 

机构地区：[1]泰山医学院附属医院,山东泰安271000

出　　处：《临床急诊杂志》2012年第3期204-206,共3页Journal of Clinical Emergency

摘　　要：目的:研究依达拉奉对心肺复苏后大鼠脑神经元的保护作用及机制。方法:随机选取SD大鼠36只,采用窒息合并冰氯化钾停跳液致大鼠心跳骤停5min后开始心肺复苏的动物模型,随机分为假手术组、常规复苏组和依达拉奉治疗组,每组12只。复苏后48h取组织标本,采用比色法测定脑组织中丙二醛(MDA)含量及超氧化物歧化酶(SOD)活力,应用原位末端标记(TUNEL)法检测脑神经细胞凋亡水平。结果:依达拉奉治疗组与常规复苏组相比,脑组织中MDA含量显著降低(P<0.05),SOD活力显著升高(P<0.05);同时依达拉奉治疗组的脑神经元凋亡水平比常规复苏组显著减少(P<0.05)。结论:依达拉奉能有效对抗心肺复苏后大鼠脑细胞的再灌注损伤,减少神经元凋亡。Objective：To observe the protective effects oI Edaravone on neuron ot brain atter caralopmmonary resuscitation （CPR） in rats. Method：Cardiac arrest was induced by asphyxiation and ice-cold KCI （0.5 tool/L）. Resuscitation started 5rain after cardiac arrest. Thirty six Sprague-Dawley rats were randomly divided into 3 groups： sham operation group, conventional treatment group and Edaravone intervendon group （n= 12）. Using the colorimetry, we analyzed the quantity of maleic dialdehyde （MDA） and enzyme activity of super oxide dis- mutase （SOD） of the brain tissues in all groups. The apoptosis of cerebral neuron were confirmed by TUNEL. Resuit：Compared with the conventional treatment group, quantity of MDA declined greatly （P〈0.05）, while the activity of SOD in cerebral neuron increased markedly in the Edaravone intervention group （P〈0.05）. The number of apoptotic neuron in the Edaravone intervention group was fewer than the conventional treatment group. Conelu- sion：Edaravone will play very positive role in the protection of cerebral neuron in rats after CPR.

关 键 词：心肺复苏 缺血再灌注损伤 依达拉奉 凋亡 

分 类 号：R654.1[医药卫生—外科学]