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Independent cerebral vasoconstrictive effects of hyperoxia and accompanying arterial hypocapnia at 1 ATA

¹Department of Anesthesia, and ²Institute for Environmental Medicine Environmental Biomedical Stress Data Center, and ³Departments of Neurology and ⁴Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104

Submitted 25 March 2003 ; accepted in final form 20 August 2003

Breathing 100% O₂ at 1 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 O₂ was breathed at 1.0 ATA decreases CBF independently of a concurrent fall in arterial PCO₂. CBF was measured in seven healthy men aged 21–62 yr by using noninvasive continuous arterial spin-labeled-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 and 6% CO₂ in air and O₂ backgrounds. Arterial PO₂ increased from 91.7 ± 6.8 Torr in air to 576.7 ± 18.9 Torr in O₂. Arterial PCO₂ fell from 43.3 ± 1.8 Torr in air to 40.2 ± 3.3 Torr in 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.

cerebral blood flow; oxygen; carbon dioxide; arterial spin-labeling; magnetic resonance; atmospheres absolute

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