TY - JOUR
T1 - Independent cerebral vasoconstrictive effects of hyperoxia and accompanying arterial hypocapnia at 1 ATA
AU - Floyd, Thomas F.
AU - Clark, James M.
AU - Gelfand, Robert
AU - Detre, John A.
AU - Ratcliffe, Sarah
AU - Guvakov, Dimitri
AU - Lambertsen, Christian J.
AU - Eckenhoff, Roderic G.
PY - 2003/12
Y1 - 2003/12
N2 - 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 PO 2 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 516.7 ± 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.
AB - 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 PO 2 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 516.7 ± 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.
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U2 - 10.1152/japplphysiol.00303.2003
DO - 10.1152/japplphysiol.00303.2003
M3 - Article
C2 - 12937024
AN - SCOPUS:0344413700
SN - 8750-7587
VL - 95
SP - 2453
EP - 2461
JO - Journal of applied physiology
JF - Journal of applied physiology
IS - 6
ER -