Hagberg H, Andersson P, Butcher S, Sandberg M, Lehmann A, Hamberger A
Neurosci Lett. 1986 Aug 4;68(3):311-6. doi: 10.1016/0304-3940(86)90508-2.
The effect of blocking N-methyl-D-aspartate (NMDA)-sensitive excitatory amino acid (EAA) receptors during brain ischemia was studied in order to test a link between EAAs and neuronal energy metabolism. The receptors were blocked unilaterally in the rat striatum before, during and after an ischemic insult. The receptor blocker, D-2-amino-5-phosphonovalerate (D-APV) was administered by dialysis perfusion, which also allowed continuous sampling for analysis of adenosine triphosphate degradation products, i.e. purine catabolites, in control and D-APV-treated striata. Purine catabolites were analysed with reversed-phase liquid chromatography. Hypoxanthine, xanthine, inosine and adenosine increased dramatically in the striatum during ischemia and reached maximum levels during early reperfusion. D-APV reduced the extracellular accumulation of all measured purine catabolites during ischemia/reflow and improved to some extent the recovery of the striatal electroencephalographic activity in the majority of the animals. The results suggest that NMDA receptor blockade attenuates acute changes in energy metabolism during ischemia.
为了检验兴奋性氨基酸（EAA）与神经元能量代谢之间的联系，研究了在脑缺血期间阻断N-甲基-D-天冬氨酸（NMDA）敏感的兴奋性氨基酸（EAA）受体的作用。在缺血性损伤之前、期间和之后，在大鼠纹状体中单侧阻断这些受体。受体阻滞剂D-2-氨基-5-磷酸戊酸（D-APV）通过透析灌注给药，这也允许对对照和D-APV处理的纹状体中的三磷酸腺苷降解产物（即嘌呤分解代谢物）进行连续取样分析。嘌呤分解代谢物用反相液相色谱法分析。缺血期间纹状体中的次黄嘌呤、黄嘌呤、肌苷和腺苷显著增加，并在早期再灌注期间达到最高水平。D-APV减少了缺血/再灌注期间所有测量的嘌呤分解代谢物的细胞外积累，并在大多数动物中在一定程度上改善了纹状体脑电图活动的恢复。结果表明，NMDA受体阻断可减轻缺血期间能量代谢的急性变化。
