Magnesium Deficiency Exacerbates and Pretreatment Improves Outcome Following Traumatic Brain Injury in Rats: 31P Magnetic Resonance Spectroscopy and Behavioral Studies
Magnesium Deficiency Exacerbates and Pretreatment Improves Outcome Following Traumatic Brain Injury in Rats: 31P Magnetic Resonance Spectroscopy and Behavioral Studies
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DOI：
10.1089/neu.1988.5.17
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发表时间：
1988-01-01
影响因子：
4.2
通讯作者：
Vink, Robert
中科院分区：
文献类型：
--
作者：
McIntosh, Tracy K.;Faden, Alan I.;Vink, Robert
中枢神经系统创伤后介导迟发性或继发性组织损伤的生化机制仍然是推测性的。我们以前已经证明，大鼠创伤性脑损伤导致组织细胞内游离镁[Mg]（f）和总镁[Mg]（t）浓度迅速下降，这与损伤严重程度显著相关。为了研究镁和创伤性脑损伤之间的关系，我们评估了在大鼠液压脑损伤（2.0-2.4 atm）后，镁缺乏是否会加重或镁治疗是否会改善创伤后结局。通过磷（P-31）磁共振波谱（MRS）测量，给予缺镁饮食14天的动物显示脑[Mg]（f）降低15%。与正常喂食生理盐水的对照组相比，镁缺乏显著加重了神经功能障碍，并增加了损伤后的死亡率。相反，在脑损伤前15分钟用硫酸镁（0.1 mEq）预处理可防止生理盐水处理动物中P-31 MRS观察到的[Mg]（f）下降，并显著改善细胞生物能量状态和慢性创伤后神经功能结局。这些综合观察结果表明，创伤后脑[Mg]（f）的变化可能在创伤性脑损伤的病理生理学中发挥作用。
The biochemical mechanisms mediating delayed or secondary tissue injury after central nervous system trauma remain speculative. We have demonstrated previously that traumatic brain injury in rats causes a rapid decline in tissue intracellular free magnesium [Mg](f) and total magnesium [Mg](t) concentrations, which were significantly correlated with injury severity. In order to examine the relationship between magnesium and traumatic brain injury, we assessed whether (1) magnesium deficiency exacerbates or (2) magnesium treatment improves posttraumatic outcome following fluid-percussion brain injury (2.0-2.4 atm) in rats. Animals placed on magnesium-deficient diet for 14 days showed a 15% decrease in brain [Mg](f) as measured by phosphorus (P-31) magnetic resonance spectroscopy (MRS). Magnesium deficiency significantly exacerbated neurologic dysfunction and increased mortality following injury when compared to normally fed saline-treated controls. Conversely, pretreatment with magnesium sulfate (0.1 mEq) 15 min before brain injury prevented the fall in [Mg](f) observed by P-31 MRS in saline-treated animals and significantly improved both cellular bioenergetic state and chronic posttraumatic neurologic outcome. These combined observations suggest that alterations in brain [Mg](f) after trauma may play a role in the pathophysiology of traumatic brain injury.