Faden A I, Demediuk P, Panter S S, Vink R
Department of Neurology, University of California, San Francisco.
Science. 1989 May 19;244(4906):798-800. doi: 10.1126/science.2567056.
Brain injury induced by fluid percussion in rats caused a marked elevation in extracellular glutamate and aspartate adjacent to the trauma site. This increase in excitatory amino acids was related to the severity of the injury and was associated with a reduction in cellular bioenergetic state and intracellular free magnesium. Treatment with the noncompetitive N-methyl-D-aspartate (NMDA) antagonist dextrophan or the competitive antagonist 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid limited the resultant neurological dysfunction; dextrorphan treatment also improved the bioenergetic state after trauma and increased the intracellular free magnesium. Thus, excitatory amino acids contribute to delayed tissue damage after brain trauma; NMDA antagonists may be of benefit in treating acute head injury.
大鼠液压冲击诱导的脑损伤导致创伤部位附近细胞外谷氨酸和天冬氨酸显著升高。兴奋性氨基酸的这种增加与损伤的严重程度相关，并与细胞生物能状态降低和细胞内游离镁减少有关。用非竞争性N-甲基-D-天冬氨酸（NMDA）拮抗剂右啡烷或竞争性拮抗剂3-（2-羧基哌嗪-4-基）丙基-1-膦酸治疗可限制由此产生的神经功能障碍；右啡烷治疗还改善了创伤后的生物能状态并增加了细胞内游离镁。因此，兴奋性氨基酸促成脑创伤后延迟性组织损伤；NMDA拮抗剂可能有助于治疗急性头部损伤。
