摘要
目的:探讨极化液(GIK)联合托拉塞米对外伤后脑水肿与神经元功能恢复的影响。方法:Glasgow评分(GCS)选取6～8分、9～11分、12～14分各30人共90例脑外伤患者,每等级随机选择10例分配至对照组、GIK治疗组及GIK联合托拉塞米组,每组30人。第3天和第14天复查头颅MRI,第2天和第14天测空腹血C-反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)、白细胞(WBC)、中性粒细胞百分比(N%),丙二醛(MDA)和超氧化物歧化酶(SOD)水平,第14天行脑电图检查、重新评定GCS。结果:第14天GIK治疗组和GIK联合托拉塞米组CRP、TNF-α、IL-6、WBC、N%及MDA水平明显低于对照组(P<0.01),血清SOD明显高于对照组(P<0.01),GIK治疗组与GIK联合托拉塞米组无显著差异(P>0.05);第2天各组间以上指标无显著差异(P>0.05)。第14天GIK联合托拉塞米组脑水肿恢复、脑电图恢复、GCS进步明显优于其他两组。结论:GIK联合托拉塞米可能通过降低炎症反应、抗氧化、降低受损神经细胞兴奋性及脱水利尿等作用,有效降低外伤后脑水肿,促进神经元功能恢复。
Objective：To explore the effect of the GIK united torasemide on traumatic brain edema and recovery of neuronal function.Methods：Ninety patients with craniocerebral injury were randomly divided into control group,GIK group and group of GIK united torasemide according to different grades of Glasgow coma score.Each group had totally 30 patients including ten people with 3～8 score,10 with 9～11 score and 10 with 12～14 score.The head MRI was performed after 3 days and 14 days;the levels of the CRP,TNF-α,IL-6,white blood cell（WBC）,neutrophil,SOD and MDA were measured on the 2 nd day and 14 th day;the EEG,Glasgow score was analyzed on the 14 th day.Results：The levels of the CRP,TNF-a,IL-6,WBC,neutrophil and MDA in the GIK group and the group of GIK united torasemide were significantly lower than those in the control group（P 0.01）,while the level of the SOD in the GIK group and the group of GIK united torasemide was significantly higher than that in the control group（P0.01）,and the GIK group was not significantly different from the group of GIK united torasemide.The indexes mentioned above were not significantly different in every group on the second day.The levels of cerebral edema,the EEG,the Glasgow coma score in the group of GIK united torasemide were significantly better than others groups on the 14 th day.Conclusion：By reducing inflammatory cytokines and the excitability of the damaged neurons,anti-oxidation and dehydration,the treatment of GIK united torasemide can significantly reduce traumatic brain edema and promote recovery of neuronal function.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2010年第7期1005-1008,共4页
Journal of Nanjing Medical University(Natural Sciences)
