NMDA-antagonists reverse increased hypoxic tolerance by preceding chemical hypoxia
NMDA-antagonists reverse increased hypoxic tolerance by preceding chemical hypoxia
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DOI：
10.1016/0304-3940(96)12915-3
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发表时间：
1996-08-23
影响因子：
2.5
通讯作者：
Riepe, MW
中科院分区：
文献类型：
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作者：
Kasischke, K;Ludolph, AC;Riepe, MW
谷氨酸拮抗剂减轻急性能量代谢抑制引起的低氧损伤，本研究的目的是探讨谷氨酸拮抗剂对预先化学抑制能量代谢诱导的低氧耐受增强的影响。对照组动物脑片(缺氧15min，恢复45min)的群体峰电位(PSAP)恢复率为起始值的30%，而体内轻度化学缺氧动物制备的脑片(p切片)，经20 mg/kg 3-硝基丙酸处理后，其恢复率超过90%。在低氧前45min用D(-)-2-氨基-5-膦戊酸(APV)(100 MU M)灌流5min，复苏率下降到42+/-13%(平均+/-扫描电子显微镜)。6-氰基-7-硝基-2，3-二酮(CNQX)(10 MU)灌流后缺氧恢复率为72+/-15%(P<；0.05)。我们的结论是，N-甲基-D-天冬氨酸(NMDA)拮抗剂可以消除缺氧耐受性的增加，但非NMDA拮抗剂不能。
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 mu M) 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 mu M) 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.