期刊文献+

外源性镁离子对重型颅脑创伤患者的治疗作用 被引量:26

A study of the effect of extrinsic ionized magnesium treatment in the patients with severe traumatic brain injury
原文传递
导出
摘要 目的探讨重型颅脑创伤(sTBI)患者硫酸镁治疗与患者血清丙二醛(MDA)含量及预后的关系。方法 54例人选病例按入院先后随机分为治疗组和对照组。治疗组首先15min内静脉滴注2.5g硫酸镁,接着10g硫酸镁24h持续静滴,连用3天。对照组除硫酸镁外其他治疗完全相同。两组再按人院GCS评分分为特重组(GCS 3—5分)和重型组(GCS 6~8分),住院期间监测患者血清镁和MDA含量,伤后3个月纪录患者GOS评分。结果治疗组MDA含量低于对照组,特重组MDA含量高于重型组,血清镁离子含量低于重型组(P<0.05)。治疗组GOS评分好于对照组, 但没有统计学意义。结论分sTBI患者,伤情越重,血清MDA含量越高,血清镁离子含量越低。硫酸镁能降低sTBI患者血清MDA含量,有改善预后的趋势。 Objective To investigate the relationship between MgSO4 therapy and serum Methylene dianiline (MDA) , outcome in the patients with severe traumatic brain injury (sTBI) . Methods A prospective randomized single-blind clinical trial of MgSO4 therapy was performed in 54 cases of the patients with sTBI who were enrolled within 12 hours after injury, and given intravenous MgSO4 in the treatment group, which was initiated with a bolus of 2.5g in a 100ml solution of 0.9% NaCl over 15 minutes, followed by continuous infusion at 0.4g/hour (10g in a 500rnl solution of 0.9% NaCl at 22.5 ml/hour) for 3 days. In control group, clinical management principles were the same as treatment group except MgSO4. the Two group were subdivided into sTBI group (GCS 6-8) and special severe traumatic brain injury (ssTBI) group (GCS 3-5). Daily serum Mg^2+ and MDA were monitored, and clinical outcomes were valued using the Glasgow Outcome Scale score (GOSs) at 3 months after injury. Results Decreased serum MDA were observed in the patients with treatment group compared to control group and sTBI group compared to ssTBI group (P〈 0.05). In ssTBI group, serum Mg^2+ is lower than sTBI group (P〈 0.05). There was a slight but not significantly better GOS score in treatment group compared to control group. Conclusion The severer TBI is, the lower serum Mg^2+ and the higher serum MDA are. Intravenous MgSO4 can significantly reduce their serum MDA. Mg^2+ may act as a neuroprotective agent, and there is a trend of improving these patients' outcome.
出处 《中华神经外科杂志》 CSCD 北大核心 2006年第2期76-78,共3页 Chinese Journal of Neurosurgery
关键词 硫酸镁 重型颅脑创伤 丙二醛 预后 临床试验 MgSO4 sTBI MDA Outcome Clinical trial
  • 相关文献

参考文献10

  • 1Vink R, Mcintosh TK, Demediuk P, et al. Decline in intracellular free Mg^2+ is associated with irreversible tissue injury after brain trauma. J Biol Chem, 1988, 263: 757-761.
  • 2Hallak M, Irtenkauf SM, Cotton DB. Effect of magnesium sulfate on excitatory amino acid receptors in the rat brain. I.N-Methyl-D-Aspartate receptor channel complex. Am J Obstet Gynecol, 1996, 175 (3 Pt 1): 575-581.
  • 3Kato T. Role of magnesium ions on the regulation of NMDA receptor-a pharmacopathology of memantine. Clin Calcium,2004, 14: 76-80.
  • 4McDonald JW, Silverstein FS, Johnston MV. Magnesium reduces N-methyl-D-aspartate (NMDA) -mediated brain injury in pefinatal rats. Neurosei Lett, 1990, 109: 234-238.
  • 5Krueger RC, Santore MT, Dawson G, et al. Increased extracellular magnesium modulates proliferation in fetal neural cells in culture. Brain Res Dev Brain Res, 2001, 127: 99-109.
  • 6Kahraman S, Ozgurtas T, Kayali H, et al. Monitoring of serum ionized magnesium in neurosurgical intensive care unit:preliminary results. Clin Chim Acta, 2003, 334: 211-215.
  • 7Lewen A, Matz P, Chan PH. Free radical pathways in CNS injury. J Neurotrauma, 2000, 17: 871-890.
  • 8Halestrap AP, Woodfield KY, Connem CP. Oxidative stress,thiol reagents, and membrane potential modulate the mitochondrial permeability transition by affecting nucleotide binding to the adenine nucleotide translocase. J Biol Chem, 1997, 272:3346-3354.
  • 9Altura BM, Gebrewold A, Zhang A, et al. Low extracellular magnesium ions induce lipid peroxidation and activation of nuclear factor-kappa B in canine cerebral vascular smooth muscle: possible relation to traumatic brain injury and strokes.Neurosci Lett, 2003, 341: 189-192.
  • 10Cernak I, Savic V J, Kotur J, et al. Characterization of plasma magnesium concentration and oxidative stress following graded traumatic brain injury in humans.J Neurotrauma, 2000, 17:53-68.

同被引文献228

引证文献26

二级引证文献84

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部