Millet Y, Joanny P, Garron J, Tognetti P, Corriol J
Resuscitation. 1979;7(2):127-34. doi: 10.1016/0300-9572(79)90007-8.
Pyridoxylase at a concentration of 0.6 mmol/kg body weight injected intraperitoneally in rats, increased the resistance of animals to severe hypoxia (O2:3.2%; N2; 96.,%). The electrocorticogram (ECoG) was used to indicate the effectiveness of the drug in lowering the delay of electrographic silence, in 19 control rats and 12 pretreated rats. The ECoG was also recorded period under pure oxygen. In pretreated rats, the ECoG records became flat in a mean time of 551 s, compared with 269 s in the control group. The latent periods of successive steps during cerebral anoxia were significantly delayed in pyridoxylate-pretreated rats subjected to hypoxia. During the recovery period, pyridoxylate improved the recovery of the normal ECoG, particularly when values were expressed as a function of the duration of the hypoxic period. These findings are in good agreement with the significant protection afforded by pyridoxylate on the cerebral rate of energy-rich phosphate bond utilization during hypoxia studied in a separate work.
以0.6毫摩尔/千克体重的浓度腹腔注射给大鼠的吡哆醛酶，提高了动物对严重缺氧（氧气：3.2%；氮气：96.8%）的抵抗力。在19只对照大鼠和12只预处理大鼠中，使用脑电图（ECoG）来表明该药物在缩短脑电图沉默延迟方面的有效性。还在纯氧条件下记录了ECoG。在预处理大鼠中，ECoG记录平均在551秒时变平，而对照组为269秒。在缺氧的吡哆醛预处理大鼠中，脑缺氧期间连续步骤的潜伏期显著延迟。在恢复期，吡哆醛改善了正常ECoG的恢复，特别是当将数值表示为缺氧期持续时间的函数时。这些发现与在另一项研究中吡哆醛在缺氧期间对富含能量的磷酸键利用脑速率提供的显著保护高度一致。
