肾上腺素对心肺复苏后大鼠脑损伤研究的干扰作用  

Changes of cerebral edema after cardiopulmonary resuscitation and effect of adrenaline

作　　者：李章平[1] 陈寿权[1] 于华众[2] 王珊珊[1] 黄唯佳[1] 程俊彦[1] 王万铁[3] 王为[3] 

机构地区：[1]温州医学院附属第一医院急诊科,浙江温州325000 [2]温州医学院附属第二医院内分泌科 [3]温州医学院病理生理教研室

出　　处：《中国急救医学》2006年第2期120-122,共3页Chinese Journal of Critical Care Medicine

基　　金：温州市科技计划重点项目(Y2004A002;S2002A020)

摘　　要：目的观察大鼠心肺复苏早期脑水肿与血脑屏障变化的特点以及肾上腺素对其的干扰作用。方法以SD大鼠建立心肺复苏模型,120只大鼠随机分成手术对照组(分气管切开后即刻,1/2、3、69、h),肾上腺组(给药后即刻,1/2、3、6、9 h),复苏组(分复苏后即刻,1/2、3、69、h),检测各组脑组织水含量及EB含量,观察心肺复苏后各时点脑水肿及血脑屏障通透性的变化情况。结果大鼠注射肾上腺素后3 min内均出现心率加快,同时并发心律失常。肾上腺素组1/2 h开始出现脑组织水含量的升高,6 h已下降,9 h已基本降至基线。肾上腺素组9 h内均未出现EB含量升高。心肺复苏组于复苏后1/2 h起就出现脑组织水含量的持续增加,与手术对照组同时间点比较均P<0.01,和肾上腺素组比较6 h开始才有显著差别,同时,心肺复苏组6 h后EB含量升高,与手术对照组比较均P<0.01,与肾上腺素组比较6 hP<0.05,9 hP<0.01、相关分析发现,6 h后EB含量和脑水肿明显相关(r=0.832,P<0.01)。结论应用肾上腺素的心肺复苏早期就出现脑水肿,开始以细胞毒性脑水肿为主,而后血脑屏障开放,促使血管源性脑水肿形成,肾上腺素能一过性地促进细胞性脑水肿的形成,可能是心肺复苏早期细胞毒性脑水肿形成的主要因素,反复应用会干扰心肺复苏后早期脑水肿的研究。Objective To study the change of cerebral edema and blood - brain barrier （BBB） opening at different time points after eady cardiopuhnonary resuscitation（ CPR）, and investigate the effects of adrenalinc（AD） on cerehral edema. Methods 120 male SD rats were randomly divided into 15 groups（ n = 8, in caeh） ： sham- operation group, CPR group and adrenaline （ AD） group which were further divided into 5 subgroups respectively on the basis of time. The contents of Evens Blue （ EB） and brain water in ecrebral tissue were assayed. Results All the rats showed fast heart rate and arrhythmia three minutes afiler AD injection. In AD group, transient cerebral edema was obvious at 1/2 h after AD injection and descended gradually, however there was little ehange in the contents of EB during 9 h. The cerebral edema obviously elevated at 1/2 h after CPR, and continuously elevated at 9 h, compared with sham-operation group P 〈 0.01, compared with adrenaline group P 〈 0.01 at 6 and 9 h. BBB pemeability increased at 6h and 9 h, compared with sham - operation group P 〈 0.01, compared with adrenaline group P 〈 0.05 at 6 h and P 〈 0.01 at 9h. There were, n,arked ton＇elation between the contents of EB and brain water in cerebral tissue after 6h （ r = 0. 832, P 〈 0.01 ）. Conclusion CPR results in cytotoxic edema primarily and the increased pemeability of BBB subsecquendy, vasogenic edema plays a critical role in cerebral edema formation. AD can cause transient cytotoxic edema and interfere with the research of cerebral edema after CPR.

关 键 词：脑水肿 血脑屏障 心肺复苏术 肾上腺素 

分 类 号：R459.7[医药卫生—急诊医学]