Oxygen Toxicity. Effects in Man of Oxygen Inhalation at 1 and 3.5 Atmospheres Upon Blood Gas Transport, Cerebral Circulation and Cerebral Metabolism

Abstract

The effects of O2 inhalation at 1 and 3 to 4 atm. ambient pressure upon blood O2 and CO2 transport, cerebral circulation and cerebral metabolism were studied in normal men. At 3.5 atm., O2 inhalation produced a 55% increase in cerebral vascular resistance resulting in a 25% reduction in the rate of blood flow through the brain. Although these changes were approx. twice as great as those associated with O2 inhalation at 1 atm., the differences were not statistically significant in this small series. The amt. of O2 physically dissolved in arterial blood at 3.5 atm. averaged 6.5 vol. %, or slightly greater than the normal cerebral arteriovenous O2 difference during air breathing at 1 atm. Nevertheless, due to the slower rate of cerebral circulation, more O2 was given up to brain tissue than was present in physical soln. in the arterial blood. As a result the avg. internal jugular hemoglobin saturation at 3.5 atm. was 89%. The removal of most of the physically dissolved O2 produced a fall in pO2 of about 2000 mm. Hg as blood passed through the brain. Partial interference with the normal reduction of oxyhemoglobin rendered less efficient the transport of CO2 by the blood. Together with the diminished cerebral blood flow this accounted for an 8-mm. Hg increase in the arteriovenous pCO2 difference across the brain at 3.5 atm. of O2. Due to a 5-mm. Hg fall in arterial pCO2 the elevation of internal jugular pCO2 was limited to 3 mm. Hg. This is not compatible with the concept of a marked increase in brain tissue pCO2 as a contributing cause of O2 toxicity. No alteration in the rate of O2 consumption or the R. Q. of the brain could be detected at 1 or 3.5 atm. of inspired O2. The relationships of these findings to in vivo and in vitro studies of O2 toxicity and to respiratory stimulation by O2 are discussed. It is proposed that central accumulation of CO2 on O2 breathing at increased ambient pressures does not contribute to the toxicity of O2 but rather may indirectly reduce the exposure of brain tissue to toxic levels of O2 tension by producing hyperventilation and cerebral vasoconstriction.