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

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

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

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. METHODS: 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.