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1 Department of Anesthesiology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
2 Institute for Environmental Medicine, Environmental Biomedical Stress Data Center, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
3 Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
4 Department of Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
* To whom correspondence should be addressed. E-mail: floydt{at}uphs.upenn.edu.
Breathing 100% O2 at one atmosphere absolute (ATA) is known to be associated with a decrease in cerebral blood flow (CBF). It is also accompanied by a fall in arterial pCO2 leading to uncertainty as to whether the cerebral vasoconstriction is totally or only in part caused by arterial hypocapnia. We tested the hypothesis that the increase in arterial pO2 while breathing O2 at 1.0 ATA decreases CBF independently of a concurrent fall in arterial pCO2. CBF was measured in 7 healthy men aged 21-62 years, using noninvasive CASL-Perfusion MRI. The tracer in this technique, magnetically labeled protons in blood, has a half-life of seconds, allowing repetitive measurements over short time frames without contamination. CBF and arterial blood gases were measured while breathing air, 100% O2, and 4% CO2 and 6% CO2 in air and O2 backgrounds. Arterial pO2 increased from 91.7 ± 6.8 torr on air to 576.7 ± 18.9 torr on O2. Arterial pCO2 fell from 43.3 ± 1.8 torr on air to 40.2 ± 3.3 torr on O2. CBF-arterial pCO2 response curves for the air and hyperoxic runs were nearly parallel and separated by a distance representing a 28.7-32.6% decrement in CBF. Regression analysis confirmed the independent cerebral vasoconstrictive effect of increased arterial pO2. The present results also demonstrate that the magnitude of this effect at 1.0 ATA is greater than previously measured.
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