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

Central nervous system (CNS) oxygen toxicity can occur as convulsions and l oss of consciousness. without any premonitory symptoms. We have made a quan titative study of the effect of inspired carbon dioxide on sensitivity to o xygen 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 diox ide (PCO2) in the range 0-12 kPa until the appearance of the electroencepha lograph first electrical discharge (FED) that preceeds the clinical convuls ions. Exposures were conducted at a thermoneutral temperature of 27 degrees 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 ce rebral 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 decre ased with the increase in PO2. This log-linear relationship made possible t he derivation of equations that describe latency to the FED as a function o f both PO2 and PCO2 in the PCO2 - dependent range: Latency (min) = e((5.19- 0.0040PO2)) - e((2.77-0.0034PO2)) X PCO2 (kPa), and in the PCO2-independent range: Latency(min) = e((2.44-0.0009PO2)). A PCO2 as low as 1 kPa signific antly reduced the latency to the FED. It is suggested that in closed-circui t oxygen diving, any accumulation of carbon dioxide should be avoided in or der to minimize the risk of CNS oxygen toxicity.