Recovery time constant in central nervous system O2 toxicity in the rat.

Abstract

The development of oxygen toxicity can be delayed by intermittent periods of normoxia. However, there is no accepted procedure for quantifing the recovery during normoxia. A cumulative oxygen toxicity index - K, when K reaches a critical value (Kc) and the toxic effect is manifested, can be calculated using the equation K = t(2)e x PO(2)c where t(e) is hyperoxic exposure time and PO2 is oxygen pressure and c is a power parameter. Recovery during normoxia (reducing K) is calculated by the equation K2 = K1 x 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 PO2 = 608 kPa followed by a period of normoxia (3.5% O2), with a subsequent return to PO2 = 608 kPa until appearance of the first electrical discharge (FED) in the electroencephalogram which precedes clinical convulsions. In protocol B (n = 22), 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.