[abstract] ALTERATIONS IN SEIZURE MECHANISMS BY OXYGEN HIGH PRESSURE USING 1,1-DIMETHYLHYDRAZINE AND PYRIDOXINE.

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[abstract] ALTERATIONS IN SEIZURE MECHANISMS BY OXYGEN HIGH PRESSURE USING 1,1-DIMETHYLHYDRAZINE AND PYRIDOXINE.

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Title: [abstract] ALTERATIONS IN SEIZURE MECHANISMS BY OXYGEN HIGH PRESSURE USING 1,1-DIMETHYLHYDRAZINE AND PYRIDOXINE.
Author: Segerbo, BE
Abstract: Oxygen high pressure (OHP) and 1,1-dimethylhydrazine (UDMH) both cause grand mal seizures, brain glycogen degradation and inhibition of glutamic acid decarboxylase (GAD). Brain glycogen degradation in a sudden process was possibly initiated by the convulsions in the case of UDMH-poisoning. However, a gradual decrease was detectable well before the onset of toxicity symptoms when OHP was used. UDMH-inj. causes consecutive convulsions that follow a predictable sequence. The time to convulsions is generally referred to as the induction period and the time in between as the refractory period. After a single inj. of UDMH there was a gradual decrease in resistance to OHP during the induction period measured as time to convulsions at 6 ATA 100% oxygen and in the refractory period this time was only 4 min. with a control value of 26 min. for non treated rats. Administration of Pyridoxine, a B-vitamine, 2 hours after UDMH-inj. in the refractory period, resulted in an immediate tenfold increase in resistance to oxygen toxicity, from 4 min. to 45 min. Pyridoxine is known to reverse inhibition of UDMH on GAD and there is possibly an accumulation of substrate when GAD-inhibition is diminishing. Simu1taneous inj. of Pyridoxine and UDMH caused no spontaneous convulsions, unchanged brain glycogen levels and unchanged or increased resistance to OHP measured two or three hours after inj.
URI: http://archive.rubicon-foundation.org/4287
Date: 1978

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  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

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