肾上腺素对心肺复苏后大鼠脑损伤研究的干扰作用

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、6、9h），肾上腺组（给药后即刻，1／2、3、6、9h），复苏组（分复苏后即刻，1／2、3、6、9h），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3min内均出现心率加快，同时并发心律失常。肾上腺素组1／2h开始出现脑组织水含量的升高，6h已下降，9h已基本降至基线.肾上腺素组9h内均未出现EB含量升高.心肺复苏组于复苏后1／2h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6h开始才有显著差别，同时，心肺复苏纽6h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6hP〈0．05，9hP〈0．01、相关分析发现，6h后EB舍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。

Changes of cerebral edema after cardiopulmonary resuscitation and effect of adrenaline

Objective To study the change of cerebral edema and blood-brain barrier(BBB) opening at different time points after early cardiopulmonary resuscitation(CPR),and investigate the effects of adrenaline(AD) on cerebral edema.Methods 120 male SD rats were randomly divided into 15 groups(n=8,in each) : 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 cerebral tissue were assayed.Results All the rats showed fast heart rate and arrhythmia three minutes after AD injection.In AD group,transient cerebral edema was obvious at 1/2 h after AD injection and descended gradually,however there was little change 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 permeability 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 9 h.There were marked correlation 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 permeability of BBB subsequently,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.