Latency to CNS oxygen toxicity in rats as a function of PCO₂ and PO₂

Abstract

Central nervous system (CNS) oxygen toxicity can occur as convulsions and loss of consciousness, without any premonitory symptoms. We have made a quantitative study of the effect of inspired carbon dioxide on sensitivity to oxygen toxicity in the rat. Rats were exposed to four oxygen pressures (PO₂; 456, 507, 608 and 709 kPa) and an inspired partial pressure of carbon dioxide (PCO₂) in the range 0–12 kPa until the appearance of the electroencephalograph first electrical discharge (FED) that preceds the clinical convulsions. Exposures were conducted at a thermoneutral temperature of 27°C. Latency to the FED decreased linearly with the increase in PCO₂ at all four PO₂ values studied. This decrease, which is probably related to the cerebral vasodilatory effect of carbon dioxide, reached a minimal value that remained constant on further elevation of PCO₂. The slopes (absolute value) and intercepts of latency to the FED as a function of carbon dioxide decreased with the increase in PO₂. This log-linear relationship made possible the derivation of equations that describe latency to the FED as a function of both PO₂ and PCO₂ in the PCO₂– dependent range: Latency (min) = e^{(5.19−0.0040 P O2)}−e^{(2.77−0.0034 P O2)} × PCO₂ (kPa), and in the PCO₂-independent range: Latency(min) = e^{(2.44−0.0009 P O2)}. A PCO₂ as low as 1 kPa significantly reduced the latency to the FED. It is suggested that in closed-circuit oxygen diving, any accumulation of carbon dioxide should be avoided in order to minimize the risk of CNS oxygen toxicity.