Kasischke K, Ludolph A C, Riepe M W
Department of Neurology, Humboldt University, Berlin, Germany.
Neurosci Lett. 1996 Aug 23;214(2-3):175-8. doi: 10.1016/0304-3940(96)12915-3.
Glutamate antagonists mitigate hypoxic damage upon acute inhibition of energy metabolism. The goal of this study was to investigate their effect on increased hypoxic tolerance induced by preceding chemical inhibition of energy metabolism. While recovery of population spike amplitude (psap) is 30% of onset in slices prepared from control animals (15 min hypoxia, 45 min recovery), recovery exceeds 90% in slices prepared from animals that underwent mild chemical hypoxia in vivo by treatment with 20 mg/kg 3-nitropropionic acid 1 h prior to slice preparation (p-slices). In p-slices perfused for 5 min with D(-)-2-amino-5-phosphonopentanoic acid (APV) (100 microM) 45 min prior to hypoxia, recovery declines to 42 +/- 13% (mean +/- SEM). In contrast, posthypoxic recovery after similar perfusion with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM) is 72 +/- 15% (P < 0.05). We conclude that increased hypoxic tolerance is abolished by N-methyl-D-aspartate (NMDA)-antagonists but not non-NMDA-antagonists.
谷氨酸拮抗剂可减轻能量代谢急性抑制时的缺氧损伤。本研究的目的是探讨它们对先前能量代谢化学抑制所诱导的缺氧耐受性增加的影响。在对照动物制备的切片中（15分钟缺氧，45分钟恢复），群体峰电位幅度（psap）的恢复为起始值的30%，而在切片制备前1小时经20mg/kg 3-硝基丙酸体内轻度化学缺氧处理的动物制备的切片中（p切片），恢复超过90%。在缺氧前45分钟用D-（-）-2-氨基-5-膦酰戊酸（APV）（100μM）灌注5分钟的p切片中，恢复率降至42±13%（平均值±标准误）。相比之下，用6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）（10μM）进行类似灌注后的缺氧后恢复率为72±15%（P<0.05）。我们得出结论，N-甲基-D-天冬氨酸（NMDA）拮抗剂可消除增加的缺氧耐受性，而非NMDA拮抗剂则不能。
