Segerbo B
J Neurochem. 1981 Nov;37(5):1125-9. doi: 10.1111/j.1471-4159.1981.tb04662.x.
A study was made to test the influence of rapid variations in glutamic acid decarboxylase (GAD) activity on the susceptibility of rats to hyperbaric oxygen (HBO). GAD was inhibited by the convulsant drug unsymmetrical dimethylhydrazine (UDMH) and reactivated by pyridoxine (PYR) after onset of convulsive activity. There was a relatively long induction period after UDMH injection until the onset of convulsions and the predictable interictal periods between successive periodic convulsions made it possible to study the impact of variations in GAD activity on survival rates, suspectibility to HBO and brain glycogen levels in a time sequence after UDMH administration. The experiments showed that UDMH interferes with aerobic metabolism in brain in such a way that profound alterations in resistance to acute oxygen poisoning resulted. An accumulation of substrate proximal to the enzyme block is assumed to develop during UDMH poisoning. The protective effect against HBO toxicity that was achieved after reactivation of GAD by PYR injection, as well as the rapid re-establishment of glycogen levels, is believed to speak in favour of this hypothesis.
进行了一项研究，以测试谷氨酸脱羧酶（GAD）活性的快速变化对大鼠高压氧（HBO）易感性的影响。惊厥药物不对称二甲基肼（UDMH）可抑制GAD，惊厥活动发作后，吡哆醇（PYR）可使其重新激活。UDMH注射后直到惊厥发作有一段相对较长的诱导期，连续周期性惊厥之间可预测的发作间期使得研究UDMH给药后不同时间序列中GAD活性变化对存活率、HBO易感性和脑糖原水平的影响成为可能。实验表明，UDMH以导致对急性氧中毒抵抗力发生深刻改变的方式干扰大脑中的有氧代谢。在UDMH中毒期间，假定在酶阻断近端会出现底物积累。注射PYR使GAD重新激活后所实现的对HBO毒性的保护作用，以及糖原水平的快速重建，被认为支持这一假设。
