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大量实验证实脑缺血引起过量谷氨酸的释放,后者加重缺血损伤。拮抗谷氨酸的任何机制都能改善梗塞范围。这类拮抗剂由伴同NMDA受体(N—甲基—D—天门冬氨酸)离子通道的非竞争性阻滞剂[如apti-gancl(cerestat)]、NMDA受体的谷氨酸识别部位(如selfotel)或甘氨酸识别部位(如 ACEA1021、GV150526)的竞争性扣抗剂或多胺识别位位的拮抗剂(如eliprodil)和纳通道阻滞干扰谷氨酸释放以及具有其他作用的药物(如Lubeluzole,619C89)等组成。临床经验提示某些NMDA拮抗剂使用的保护神经量(如
A large number of experiments confirmed that cerebral ischemia caused excessive release of glutamate, which aggravate ischemic injury. Any mechanism of antagonizing glutamate can improve infarct size. Such antagonists consist of a noncompetitive blocker with an NMDA receptor (N-methyl-D-aspartate) ion channel [eg apti-gancl (cerestat)], a glutamate recognition site (Such as selfotel) or glycine recognition sites (such as ACEA1021, GV150526) or antagonists of polyamine recognition sites (such as eliprodil) and nanochannel block interference with glutamate release and other drugs ( Such as Lubeluzole, 619C89) and other components. Clinical experience suggests that certain NMDA antagonists use protective neurons (eg