Hyperbaric oxygen (HBO 2 ) increases oxygen tension (PO 2 ) in blood but reduces blood flow by means of O 2 -induced vasoconstriction. Here we report the first quantitative evaluation of these opposing effects on tissue PO 2 in brain, using anesthetized rats exposed to HBO 2 at 2 to 6 atmospheres absolute (ATA). We assessed the contribution of regional cerebral blood flow (rCBF) to brain PO 2 as inspired PO 2 (PiO 2 ) exceeds 1 ATA. We measured rCBF and local PO 2 simultaneously in striatum using collocated platinum electrodes. Cerebral blood flow was computed from H 2 clearance curves in vivo and PO 2 from electrodes calibrated in vitro, before and after insertion. Arterial PCO 2 was controlled, and body temperature, blood pressure, and EEG were monitored. Scatter plots of rCBF versus PO 2 were nonlinear (R 2 ¼ 0.75) for rats breathing room air but nearly linear (R 2 ¼ 0.88-0.91) for O 2 at 2 to 6 ATA. The contribution of rCBF to brain PO 2 was estimated at constant inspired PO 2 , by increasing rCBF with acetazolamide (AZA) or decreasing it with N-nitro-L-arginine methyl ester (L-NAME). At basal rCBF (78 mL/100 g min), local PO 2 increased 7-to 33-fold at 2 to 6 ATA, compared with room air. A doubling of rCBF increased striatal PO 2 not quite two-fold in rats breathing room air but 13-to 64-fold in those breathing HBO 2 at 2 to 6 ATA. These findings support our hypothesis that HBO 2 increases PO 2 in brain in direct proportion to rCBF. IntroductionThe O 2 content of blood is the mathematical product of hemoglobin concentration and arterial hemoglobin O 2 saturation, the latter being a nonlinear function of arterial oxygen partial pressure (PaO 2 ). The small amount of O 2 dissolved in plasma is usually negligible. However, breathing hyperbaric oxygen (HBO 2 ), that is oxygen at pressures greater than 1 atmosphere absolute (ATA), raises PaO 2 beyond the point at which hemoglobin is fully saturated, so that the dissolved fraction becomes the main source of O 2 available to cells. But this does not assure enhanced O 2 delivery to brain, because tissue PO 2 also depends on regional blood flow.Tissue oxygen tension (PO 2 ) is a dynamic balance between O 2 delivery and consumption. Many authors have reported increased brain PO 2 in HBO 2 (Jamieson and Van Den Brenk, 1962;Bennett, 1965;Bean et al, 1971;Torbati et al, 1978;Hunt et al, 1978), and reviews are available (Jamieson, 1989;Camporesi et al, 1996;Dean et al, 2003). It is also known that total or regional cerebral blood flow (rCBF) decreases in HBO 2 as a function of pressure and time. But the contribution of CBF to brain PO 2 had never been quantified. Cerebral vasoconstriction and decreased total or rCBF have been shown in healthy volunteers and patients breathing O 2 at 3.5 ATA for brief periods (Lambertsen et al, 1953;Visser et al, 1996;Omae et al, 1998). In animals, in which HBO 2 is maintained for longer times and at higher pressures, the rCBF response is biphasic: the initial decrease in rCBF is followed by a secondary rise to www.jcbfm.com control leve...