氯胺酮对脑冷冻伤后自由基和脑水肿的影响

The effects of ketamine of free radical and brain edema after cold-induced injury

目的 探讨N 甲基 D 天门冬氨酸 (N methyl D aspartate,NMDA)受体非竞争性拮抗药氯胺酮对鼠脑冷冻伤后脑内超氧化物歧化酶 (superoxidedismutase ,SOD)、丙二醛 (malondi aldehyde,MDA)和脑水肿的影响。方法 4 9只SD大鼠随机分为假手术组、未治疗组和氯胺酮治疗组。采用液氮局部冷冻左侧鼠脑 30s制作冷冻伤模型 ,分别于 2、6、2 4h处死动物后 ,用分光光度法测 1 0 %脑组织匀浆中SOD活性和MDA产量。结果 脑组织含水量在冷冻伤后显著升高 ,并随时间延长而加重。氯胺酮治疗后脑组织含水量没有明显减少 ;脑组织SOD活性在 2、6h高于未治疗组 ,但 2 4h后SOD活性无显著差异。MDA含量比未治疗组在相应时段显著减少。结论 自由基是脑水肿形成的重要因素 ,氯胺酮能减轻冻伤脑组织中SOD活性的抑制 ,减少MDA生成 。

Objective To investigate the effects of ketamine on superoxide dismutase(SOD),malondialdehyde(MDA)and brain tissue water content after cold induced injury.Methods Forty nine Sprague Dawley rats were randomly divided into sham operation group,untreated group and ketamine treated group.The cold induced brain injury model of SD rats was prepared by liquid nitrogen on the dura over the left cerebral hemisphere for 30 s.After death at 2,6 and 24 hours,brain tissues were homogenized and centrifuged.SOD and MDA were assayed with spectrophotometric analysis.Results Brain tissue water content significantly increased after cold induced injury.Thereafter water content gradually elevated.Water content was no significantly decreased in ketamine treated group.SOD activity of brain tissue in ketamine treated group was significantly higher than that in untreated groups at 2 and 6 hours,respectively.But there was no significant difference between them.MDA level of brain tissue in ketamine treated group was lower than that in untreated group at 2,6 and 24 hours,respectively.Conclusion Free radicals plays an important role in the development of cerebral edema.Ketamine is effective in maintaining brain tissue SOD activity and reducing MDA,but does not reduce cerebral edema following head cold injury.