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大鼠大脑中动脉梗死和脑水肿的变化
引用本文:王桥生,方明,陈纯波,蒋鑫,朱高峰,曾红科.大鼠大脑中动脉梗死和脑水肿的变化[J].中华急诊医学杂志,2010,19(7).
作者姓名:王桥生  方明  陈纯波  蒋鑫  朱高峰  曾红科
作者单位:1. 510080,广州,广东省人民医院急危重症医学部、广东省医学科学院;南方医科大学研究生学院
2. 广东省人民医院急危重症医学部、广东省医学科学院,广州,510080
基金项目:广东省科技计划基金资助项目 
摘    要:目的 探讨大鼠永久性大脑中动脉闭塞致脑梗死和脑水肿的变化特点.方法 Sprague-Dawley雄性大鼠随机(随机数字法)分成正常组、假手术组和脑缺血组,其中脑缺血组按缺血时间分成2 h,4 h,6 h,12 h,18 h,24 h和30 h 7个亚组.线栓法制作大鼠永久性右侧大脑中动脉闭塞脑缺血模型,行2%氯化三苯基四氮唑溶液染色测量脑梗死比及干湿称重法测量脑含水量,动态观察两者的变化特点.结果 在脑缺血组,缺血4 h局部出现脑梗死灶,方差分析结果显示缺血4 h,6 h脑梗死比无差别(P=0.091);与缺血6 h相比,缺血12 h,18 h,24 h和30 h脑梗死比显著增高(P<0.01),24h达高峰.缺血4 h脑含水量开始增加,6 h后加重,24 h达高峰;缺血18 h,24 h,30 h非缺血侧脑含水量亦增高.脑水肿和脑梗死比存在显著正相关(r=0.834,P<0.01).结论 大脑中动脉闭塞6 h是脑梗死和脑水肿加重的转折点,24 h脑梗死和脑水肿达到高峰,可为临床评估脑梗死和脑水肿的病情及治疗干预的时间窗选择提供实验参考.

关 键 词:大脑中动脉闭塞  脑缺血  脑水肿  脑梗死

Analysis of the characteristic changes in cerebral infarction and cerebral edema induced by middle cerebral artery occlusion in rats
WANG Qiao-sheng,FANG Ming,CHEN Chun-bo,JIANG Xin,ZHU Gao-feng,ZENG Hong-ke.Analysis of the characteristic changes in cerebral infarction and cerebral edema induced by middle cerebral artery occlusion in rats[J].Chinese Journal of Emergency Medicine,2010,19(7).
Authors:WANG Qiao-sheng  FANG Ming  CHEN Chun-bo  JIANG Xin  ZHU Gao-feng  ZENG Hong-ke
Abstract:Objective To investigate the characteristic changes in cerebral infarction and brain edema. Method A total of 122 Healthy adult male Spraque-Dawley rats were randomly (random number) divided into three groups: normal group ( n = 12), sham operated group (n=12) and cerebral ischemia group ( n = 98). Cerebral infarction and brain edema were induced by a permanent occlusion of right middle cerebral artery (POM-CA) with ligature. According to the duration of POMCA, the rats of cerebral ischemia group were further divided into seven sub-groups, 2 h, 4 h, 6 h, 12 h, 18 h, 24 h and 30 hours. The hemispheric ratio was detected by staining with 2% 2,3,5-triphenyltetrazolium chloride solution, and brain water content was assayed by dry/wet ratio 2 h, 4 h, 6 h, 12 h, 18 h, 24 h and hours after POMCA. Results There was a focal cerebral infarction in the rats of cerebral ischemia group 4 hours after POMCA. There was no significant difference in hemispheric ratio between 4 hours and 6 hours after POMCA by One-way ANOVA (P = 0.091). Compared with 6 h sub-group, the hemispheric ratio increased significantly in 12 h, 18 h, 24 h and 30 h sub-groups (P < 0.01), and the peak was in the 24 h sub-group. The brain water content began to increase 4 hours after POMCA and aggravated 6 hours later, and reached the peak 24 hours after POMCA. The brain water content of the non-ischemic hemisphere increased 18 h,24 h and 30 hours after POMCA. Furthermore, there was a significant correlation between the hemispheric ratio and brain water content ( r = 0.834, P < 0.01). Conclusions The critical point of cerebral infarction and brain edema aggravated is 6 hours after POMCA. Both brain edema and cerebral infarction reach the most serious degree 24 hours after POMCA. It is an important experimental evidence for evaluating the milieu conducive to the pathogenesis, and choosing the suitable time window for the treatment of cerebral infarction and brain edema.
Keywords:Middle cerebral artery occlusion  Cerebral ischemia  Cerebral edema  Cerebral infarction
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