亚低温减少沙土鼠脑缺血后延迟性神经元死亡机制的研究

THE STUDY OF MECHANISM BY WHICH MILD HYPOTHERMIA REDUCED DELAYED NEURONAL DEATH AFTER CEREBRAL ISCHEMIA IN GERBILS

目的 :研究亚低温对脑缺血后延迟性神经元死亡的影响及其与海马羟自由基产生以及纹状体多巴胺和ATP含量变化的关系。方法 :沙土鼠前脑缺血再灌注模型 ,缺血 10min ,应用病理检查方法判断海马CAl锥体细胞死亡的数目。动物随机分为假手术组、缺血组、缺血再灌注组和亚低温缺血再灌注组。高效液相加电化学检测器方法测定海马羟自由基和纹状体多巴胺的含量 ,高效液相紫外检测器法测定纹状体ATP含量。结果 :亚低温条件下沙土鼠海马CA1区锥体细胞的死亡数目明显减少 ,海马 2 ,3 DHBA的含量明显低于缺血再灌注组 (P <0 .0 1) ,纹状体多巴胺和ATP含量均明显高于缺血再灌注组 (P <0 .0 1)。结论 :低温可减少脑缺血后延迟性神经元死亡的数目 。

Aim: To study the effect of mild hypothermia on delayed neuronal death as well as the relationship between hydroxyl radicals generation in hippocampus and the change of dopamine and ATP content in striatum following ischemia/reperfusion in gerbils. Me thods : The ischemia was induced by occlusion the both carotid common arteries for 10 minutes in gerbils. Animals were divided into four groups: sham operated group, ischemic group, ischemia/reperfusion group and mild hypothermic ischemia/reperfusin group. The numbers of delayed neuronal death were assessed by histological examination. OH· outputs in hippocampus and dopamine content in striatum were specifically identified and quantitated by high performance liquid chromatography (HPLC) coupled with electrochemical detection (ECD). ATP content in striatum was also determined by HPLC. Results: Mild hypothermia significantly reduced the numbers of damaged neurons in hippocampus CA1 subfield after ischemia in gerbils. In MH group, 2,3 DHBA outputs were much less than that in IR group ( P <0.01). Dopamine and ATP content in striatum were higher than those in IR group ( P <0.01). Conclusion: Mild hypothermia could decrease the delayed neuronal death in gerbils by reducing hydroxyl radicals production in hippocampus and inhibiting dopamine release as well as prompting the recovery of ATP content in striatum following ischemia/reperfusion in gerbils.