摘要
目的:动态观察新西兰兔脊髓缺血再灌注损伤延迟性瘫痪时脊髓组织超氧歧化酶(SOD)、丙二醛(MDA)的变化,探讨其临床意义。方法:20只新西兰白兔随机分为两组:假手术对照组(sham组)和缺血再灌注26min组(IR组)。两组参照并改进Zivin方法建立兔脊髓腰骶段缺血再灌注延迟性瘫痪模型,比较两组不同动物不同时间点后肢运动功能及静脉血中丙二醛(MDA)、超氧歧化酶(SOD)活性。结果:对照组中MDA、SOD没有明显变化,动物均完全康复。IR组在再灌注缺血前、再灌注2h、8h、16h、24h中,SOD含量逐渐降低,至再灌注24h最低;再灌注72h、168h后SOD逐渐恢复到缺血再灌注前水平;MDA在再灌注缺血前、再灌注2h、8h、16h、24h中,含量逐渐增高,至再灌注24h达最高;再灌注72h、168h后MDA逐渐恢复至缺血再灌注前水平。SOD与MDA的含量变化明显负相关。IR组的后肢运动功能评分在再灌注2h、8h和16h与sham组无明显差异,至再灌注24h、72h和168h后明显低于对照组,出现延迟性瘫痪,平均发生时间为19.6h。结论:自由基介导的脂质过氧化反应在脊髓缺血再灌注损伤延迟性瘫痪中具有重要作用。
ABSTRACT Objective： To dynamically observe the changes in serum Superoxide dismutase （SOD） and Maleie dialdehyde （MDA） during the spinal cord isehemia reperfusion delayed paraplegia in rabbits. Methods： Twenty New Zealand white rabbits were randomly divided into sham-operated group and ischemia reperfusion group. The rabbit models of spinal cord ischemia injury were formed by clamping abdominal aorta 26 minutes. In the ischemia reperfuslon group, the vein blood samples were collected at seven different time intervals ： before clamping the abdominal aorta, 2h, 8h , 16h ,24h , 72h , and 168h postreperfuison. The serum of Superoxide dismutase （SOD） and Maleie dialdehyde （MDA） activity were measured. Neurologic function of the rear 2imb was assessed too. Results ：At post-spinal cord ischemia of 2h, 8h, 16h and 24h, SOD activity reduced and MDA level raised gradually. The changes were returned to nomal after 72h and 168h of reperfusion. Delayed paraplegia occurred in all rabbits of isehemia reperfusion group at 16-24h. Conclusion： The study proves that the superoxide dismutase and maleie dialdehyde play an important role in spinal cord isehemia-reperfusion injury delayed paraplegia.
出处
《陕西医学杂志》
CAS
北大核心
2007年第3期265-268,共4页
Shaanxi Medical Journal
基金
陕西省卫生厅科研基金资助(04012)
