Segerbo B E
Undersea Biomed Res. 1979 Jun;6(2):167-74.
High pressure oxygen (HBO) and 1,1-dimethylhydrazine (UDMH) both cause grand mal seizures, brain glycogen degradation, and inhibition of glutamic acid decarboxylase (GAD). Brain glycogen degradation is a sudden process that is perhaps initiated by convulsions in the case of UDMH-poisoning, but a gradual decrease in glycogen is detectable before the onset of hyperbaric oxygen toxicity symptoms. UDMH injection causes consecutive convulsions that follow a predictable sequence. (Time to convulsions is referred to as the induction period, and time between convulsions as the interictal period.) After a single injection of UDMH, there is a gradual decrease in resistance to HBO during the induction period, measured as time to convulsions breathing 100% oxygen at 6 ATA; in the first interictal period, this time is only 4 1/2 min in comparison with a control value of 26 min for untreated rats. Administration of pyridoxine, a B6-vitamin, 2 h after UDMH injection in the first interictal period, resulted in an immediate tenfold increase in resistance to oxygen toxicity, from 4 1/2 to 48 min. Pyridoxine may reverse the inhibitary effect of UDMH on GAD, and there is perhaps an accumulation of substrate, which is made available when GAD inhibition is diminishing. Simultaneous injection of pyridoxine and UDMH causes no convulsions, no change in brain glycogen levels, and an unchanged or increased resistance to HBO, measured two and three hours after injection.
高压氧（HBO）和偏二甲肼（UDMH）均可导致癫痫大发作、脑糖原降解以及谷氨酸脱羧酶（GAD）受抑制。脑糖原降解是一个突然发生的过程，在UDMH中毒情况下可能由惊厥引发，但在高压氧毒性症状出现之前，糖原会逐渐减少。注射UDMH会引发一系列可预测顺序的连续惊厥。（惊厥发作时间称为诱导期，两次惊厥之间的时间称为发作间期。）单次注射UDMH后，在诱导期对HBO的耐受性会逐渐降低，以在6个绝对大气压下呼吸100%氧气至惊厥发作的时间来衡量；在第一个发作间期，与未处理大鼠的对照值26分钟相比，这个时间仅为4.5分钟。在第一个发作间期，UDMH注射2小时后给予维生素B6吡哆醇，对氧毒性的耐受性立即增加了10倍，从4.5分钟增至48分钟。吡哆醇可能会逆转UDMH对GAD的抑制作用，并且可能存在底物的积累，当GAD抑制作用减弱时底物可供利用。同时注射吡哆醇和UDMH不会引发惊厥，脑糖原水平无变化，且在注射后两小时和三小时测量时，对HBO的耐受性不变或增加。
