Kuhr W G, Korf J
Department of Biological Psychiatry, University of Groningen, The Netherlands.
Eur J Pharmacol. 1988 Oct 11;155(1-2):145-9. doi: 10.1016/0014-2999(88)90412-8.
Intracerebral dialysis in conscious freely moving rats was used to examine the involvement of the N-methyl-D-aspartate (NMDA) receptor in the formation of lactic acid and its consequent appearance in extracellular fluid. Local administration of NMDA in the striatum of conscious, freely moving rats was found to produce a transient increase in extracellular lactate. Alternatively, administration of the NMDA antagonists 2-amino-7-phosphonoheptanoic acid or 2-amino-5-phosphonopentanoic acid delayed the onset of and attenuated the magnitude of the lactate production induced by an electroconvulsive seizure. Pretreatment of the striatum with either of these antagonists reduced the total amount of lactate observed in extracellular fluid following ischemia induced by cardiac arrest, but did not affect the time course of the appearance of lactate in the extracellular space.
在清醒自由活动的大鼠中进行脑内透析，以研究N-甲基-D-天冬氨酸（NMDA）受体在乳酸形成及其随后在细胞外液中出现过程中的作用。发现在清醒自由活动的大鼠纹状体中局部给予NMDA会使细胞外乳酸短暂增加。另外，给予NMDA拮抗剂2-氨基-7-磷酸庚酸或2-氨基-5-磷酸戊酸可延迟电惊厥诱发的乳酸产生的起始并减弱其幅度。用这两种拮抗剂中的任何一种预处理纹状体，可减少心脏骤停诱导的缺血后细胞外液中观察到的乳酸总量，但不影响细胞外空间中乳酸出现的时间进程。
