Cerebral O2 in exposures to O2 at atmospheric and higher pressure, and influence of CO2

Abstract

In polarographic experiments on anesthetized dogs and rats, a shift from breathing air to breathing oxygen at atmospheric pressure, and also at a high pressure (OHP) of 5 atm, raised availability of oxygen to the brain to levels well maintained throughout the exposure (20–55 min). Decompression reversed these effects. Cerebral vasoconstriction which may have occurred in OHP was apparently insufficient to prevent pronounced elevation of cerebral O₂ or to protect against O₂ toxicity. In simultaneous recordings from two regions, the occurrence of cyclic changes, frequently out of phase, suggest the involvement of a reciprocating cerebral vascular control mechanism between different regions. Addition of CO₂ to the OHP, to give concentrations of 0.8–1.7%, usually raised the O₂ availability and tended to precipitate asynchronous cyclic O₂ changes; apparently brain vasculature does not necessarily react en masse to CO₂. The data suggest there are wide variations in Po₂, Pco₂, and pH in circumscribed regions of the brain, for which the internal jugular venous blood is not a reliable index. Such regions may serve to precipitate manifestations of O₂ toxicity.