Recovery time constant in central nervous system O2 toxicity in the rat
Arieli, R.; Gutterman, A.
European Journal of Applied Physiology and Occupational Physiology 75(2): 182-187
1997
ISSN/ISBN: 0301-5548 PMID: 9118986 Document Number: 481956
The development of oxygen toxicity can be delayed by intermittent periods of normoxia. However, there is no accepted procedure for quantifying the recovery during normoxia. A cumulative oxygen toxicity index - K, when K reaches a critical value (K-c) and the toxic effect is manifested, can be calculated using the equation K = t-e-2 times PO-2-c where t-e is hyperoxic exposure time and PO-2 is oxygen pressure and c is a power parameter. Recovery during normoxia (reducing K) is calculated by the equation K-2 = K-1 times e-rt!r where t-r is recovery time, r being the recovery time constant. A combination of accumulation of oxygen toxicity and its recovery can be used to calculate central nervous system oxygen toxicity. In protocol A (n = 25), r was calculated for rats exposed either continuously to 608 kPa oxygen or to PO-2 = 608 kPa followed by a period of normoxia (3.5% O-2), with a subsequent return to PO, = 608 kPa until appearance of the first electrical discharge (FED) in the electroencephalogram which precedes clinical convulsions. In protocol B (n = predicted latency to the FED was compared to measured latency for seven different exposures to hyperbaric oxygen (HBO), followed by a period of normoxia and further HBO exposure. Recovery followed an exponential path, with r = 0.31 (SD 0.12) min-1. The predicted latency to FED in protocol B correlated with the measured latencies. Calculation of the recovery of the CNS oxygen toxicity agreed with the previously suggested exponential recovery of the hypoxic ventilatory response and was probably a general recovery process. We concluded that recovery can be applied to the design of various hyperoxic exposures.