深低温停循环下的脑保护方法

Brain protection during deep hypothermic circulatory arrest

将10只犬随机分为对照组(A组)与脑保护液组(B组),经体外循环降温至18℃并停止全身循环2小时。B组于停循环即刻通过颈总动脉向头部灌注4℃充氧不含钾晶体液(50ml/kg),随后每30分钟再灌注一次(10ml/kg),至停循环末,复温至37℃,继续观察6小时。A组处理同B组但不灌注脑保护液。分别于五个时相取脑皮层测三磷酸腺苷(ATP)与丙二醛(MDA),并进行超微结构观察,动态记录脑电图。结果表明:A组经2小时停循环,ATP较术前明显下降(P<0.01),MDA较术前明显增加(P<0.01),脑电图恢复时间延长,电镜显示细胞受损严重。而B组以上指际均较A组有明显改善(P<0.01),脑电图恢复较快,细胞受损也明显减轻。结论:深低温并2小时的循环停止将造成神经细胞的明显损伤,应用脑保护液可显著减轻这种损伤,并延长停循环的时限。

Ten mongrel dogs,divided randomly into a control group (A) and a cerebroplegia group (B) ,were supported by closed-chest cardiopulmonary bypass,subjected to 2 hours of hypothermic circulatory arrest at 18 C. In group B, oxygenated asanguineous solution 50ml/kg was infused into the carotid artery at the onset of arrest. and 10 ml/kg was supplemented every 30 minutes during 2hours arrest. Nothing was infused in group A. Then all animals were rewarmed to 37 C and killed 6 hours later At five time points cerebral cortex was collected to study adnosine triphosphate (ATP),malondialde hyde (MDA) and ultrastructure. Electroencephalography (EEG) was recorded continuously. In group A, ATP content decreased gradually from the beginning of arrest to the end of the experiment (P<0.01), While MDA levels increased significantly at the 2 hours of arrest and 30 minutes after repefusion(P<0.01),EEG recovery returned slowly to normal after rewarming, and the ultrastructure became obviously abnormal. But in group B,all the signs were improved significantly. These results suggest that deep hypothermia with 2 hours of circulatory arrest causes critical damages to brain cells, from which the. cerebroplegia protects the brain by improving intracellular energies and reducing ischemic injuries.