摘要
目的：探讨自由基在脊髓缺血及再灌注损伤中的作用。方法：通过阻断兔腹主动脉，造成脊髓腰尾段缺血。对缺血前、缺血４０ｍｉｎ和再灌流４ｈ局部脊髓组织超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的活力、谷胱甘肽（ＧＳＨ），过氧化脂质（ＬＰＯ）的含量进行研究。结果：缺血４０ｍｉｎ，ＳＯＤ、ＧＳＨ－Ｐｘ活力及ＧＳＨ含量明显降低，ＬＰＯ含量明显升高，与缺血前比较有显著性差异（Ｐ均＜０．０１）。再灌流４ｈ，ＳＯＤ、ＧＳＨ－Ｐｘ活力及ＧＳＨ含量进一步降低，ＬＰＯ含量进一步升高，与缺血前比较Ｐ＜０．０１，与缺血４０ｍｉｎ比较Ｐ＜０．０１或＜０．０５。结论：上述结果说明缺血４０ｍｉｎ有明确的ＳＯＤ、ＧＳＨ－Ｐｘ、ＧＳＨ和ＬＰＯ改变，再灌流４ｈ上述指标改变进一步加重。自由基介导的脂质过氧化反应在脊髓缺血及缺血后再灌流损伤中具有重要作用。
Objective:This paper was to explore the effects of free radicals on ischemic spinal cord injuries. Methods:By occluding the abdominal aorta, we induced lumbosacral spinal cord ischemia in rabbits. The activity of SOD, GSH Px, and GSH, as well as the content of lipid peroxide(LPO) were measured before ischemia, when it lasted for forty minutes, and four hours after reperfusion respectively. Results:The activity of SOD, GSH Px, and GSH decreased sharply and the content of LPO increased remarkably after forty minutes of ischemia (P<0.01). The activity of SOD, GSH Px, and GSH decreased further and the content of LPO increased more after four hours of reperfusion, P<0.01 (as compared with that happened prior to ischemia), and P<0.05 (as compared with that occurred for forty minutes of ischemia). Conclusions:Definite injurious changes happened in SOD, GSH Px, GSH and LPO after 40 minutes of ischemia. The condition deteriorated after four hours of reperfusion. The effects of lipid peroxidation initiated by free radicals contributed seriously to spinal cord ischemia and postischemic reperfusion injury.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
1998年第6期607-609,616,共4页
Journal of China Medical University
