Abstract
Single exposures of high pressure oxygen (OHP) at 30–66 Ψ gauge pressure caused CNS damage and paralysis in rats and mice but guinea pigs, rabbits and man did not show such sequellae. The CNS damage in rats was greatly increased by CNS depressent drugs (pentobarbital sodium, paraldehyde, N 2O and sermyl) given before exposure to OHP. The CNS lesions were also potentiated by raised respired pCO 2, by acetazolamide and by NH 4Cl, whilst protection was afforded by methaemoglobinaemia (induced by PAPP) by the tris-buffer THAM, by 2–4 dinitrophenol and by 5HT against the barbiturate and CO 2 potentiation of OHP brain damage. OHP induced brain damage was not modified by (I) hypothermia (CP z), (II) electroconvulsive shock treatment during OHP, (III) by cerebral X-irradiation, (IV) by adrenalectomy or cortisone, (V) by slow decompression rates, (VI) by spinal block with local anaesthetic, (VII) by “conditioning” of rats to OHP, (VIII) by hyper- and hypo-glycaemia, and (IX) by alterations in tissue histamine levels. The results are discussed in relation to possible biochemical mechanisms and theories of oxygen poisoning.
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