Simon R, Shiraishi K
Department of Neurology, University of California, San Francisco.
Ann Neurol. 1990 Jun;27(6):606-11. doi: 10.1002/ana.410270604.
Pharmacological inhibition of cell excitation during focal ischemia was studied in the rat middle cerebral artery occlusion model. The potent and selective N-methyl-D-aspartate antagonist CGS 19755, administered 5 minutes prior to or 5 minutes following permanent middle cerebral artery occlusion, caused a substantial decrease in infarct size, which was associated with reduction of postischemic cerebral glucose hypermetabolism. These data support a role for excitation-induced hypermetabolism in the pathogenesis of infarction following focal cerebrovascular occlusion.
在大鼠大脑中动脉闭塞模型中,研究了局灶性缺血期间细胞兴奋的药理学抑制作用。强效且选择性的N-甲基-D-天冬氨酸拮抗剂CGS 19755,在永久性大脑中动脉闭塞前5分钟或闭塞后5分钟给药,可使梗死灶大小显著减小,这与缺血后脑葡萄糖代谢亢进的减轻相关。这些数据支持兴奋诱导的代谢亢进在局灶性脑血管闭塞后梗死发病机制中的作用。