Central nervous system (CNS) oxygen toxicity can occur as convulsions and l
oss of consciousness when hyperbaric oxygen is breathed in diving and hyper
baric medical therapy. Lin and Jamieson (J Appl Physiol 75: 1980-1983, 1993
) reported that humidity in the inspired gas enhances CNS oxygen toxicity.
Because alveolar gas is fully saturated with water vapor, we could not see
a cause and effect and surmised that other factors, such as metabolic rate,
might be involved. Rats were exposed to 507- and 608-kPa O-2 in dry (31 or
14%) or humid (99%) atmosphere until the appearance of the first electrica
l discharge preceding the clinical convulsions. Each rat served as its own
control. A thermoneutral temperature (28 +/- 0.4 degreesC) yielded resting
CO2 production of 0.81 +/- 0.06 ml.g(-1).h(-1). Latency to the first electr
ical discharge was not affected by humidity. At 507-kPa O-2, latency was 23
+/- 0.4 and 22 +/- 0.7 min in dry and humid conditions, respectively, and,
at 608-kPa O-2, latency was 15 +/- 4 and 14 +/- 3 min in dry and humid con
ditions, respectively. When no effects of CO2 and metabolic rate are presen
t, humidity does not affect CNS oxygen toxicity. Relevance of the findings
to diving and hyperbaric therapy is discussed.