Vink R, McIntosh T K, Demediuk P, Weiner M W, Faden A I
Center for Neural Injury, University of California, San Francisco 94143.
J Biol Chem. 1988 Jan 15;263(2):757-61.
Much of the tissue damage resulting from trauma to the central nervous system appears to result from secondary, delayed biochemical changes that follow primary mechanical injury. However, the early biochemical events remain to be elucidated. In the present studies, we have used phosphorus (31P) magnetic resonance spectroscopy (MRS) to examine in vivo, the temporal changes in brain intracellular free Mg2+ concentration following fluid percussion head injury in rats. We report that injury caused a profound and rapid decrease in intracellular free Mg2+ which was significantly correlated with the severity of injury. At high levels of injury, the decrease in intracellular free Mg2+ concentration was associated with a decrease in total Mg2+ concentration as determined by atomic absorption spectrophotometry. Prophylactic treatment with MgSO4 prevented the post-traumatic decrease in intracellular free Mg2+ and resulted in a significant improvement in acute neurological outcome. Because magnesium is essential for a number of critical enzyme reactions, including those of glycolysis, oxidative and substrate level phosphorylation, protein synthesis, and phospholipid synthesis, changes in free Mg2+ after brain trauma may represent a critical early factor leading to irreversible tissue damage.
中枢神经系统创伤导致的许多组织损伤似乎是由原发性机械损伤后继发的、延迟的生化变化引起的。然而，早期的生化事件仍有待阐明。在本研究中，我们使用磷（31P）磁共振波谱（MRS）在体内检测大鼠液体冲击性脑损伤后细胞内游离镁离子（Mg2+）浓度的时间变化。我们报告称，损伤导致细胞内游离Mg2+显著快速下降，这与损伤的严重程度显著相关。在高损伤水平下，通过原子吸收分光光度法测定，细胞内游离Mg2+浓度的下降与总Mg2+浓度的下降相关。硫酸镁预防性治疗可防止创伤后细胞内游离Mg2+的下降，并显著改善急性神经功能预后。由于镁对许多关键酶反应至关重要，包括糖酵解、氧化和底物水平磷酸化、蛋白质合成以及磷脂合成等反应，脑创伤后游离Mg2+的变化可能是导致不可逆组织损伤的关键早期因素。
