Cerebral Blood Flow and Brain Oxygenation in Rats Breathing Oxygen under Pressure

Abstract

Hyperbaric oxygen (HBO₂) increases oxygen tension (PO₂) in blood but reduces blood flow by means of O₂-induced vasoconstriction. Here we report the first quantitative evaluation of these opposing effects on tissue PO₂ in brain, using anesthetized rats exposed to HBO₂ at 2 to 6 atmospheres absolute (ATA). We assessed the contribution of regional cerebral blood flow (rCBF) to brain PO₂ as inspired PO₂ (PiO₂) exceeds 1 ATA. We measured rCBF and local PO₂ simultaneously in striatum using collocated platinum electrodes. Cerebral blood flow was computed from H₂ clearance curves in vivo and PO₂ from electrodes calibrated in vitro, before and after insertion. Arterial PCO₂ was controlled, and body temperature, blood pressure, and EEG were monitored. Scatter plots of rCBF versus pO₂ were nonlinear ( R² = 0.75) for rats breathing room air but nearly linear ( R² = 0.88–0.91) for O₂ at 2 to 6 ATA. The contribution of rCBF to brain PO₂ was estimated at constant inspired PO₂, 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 PO₂ increased 7- to 33-fold at 2 to 6 ATA, compared with room air. A doubling of rCBF increased striatal PO₂ not quite two-fold in rats breathing room air but 13- to 64-fold in those breathing HBO₂ at 2 to 6 ATA. These findings support our hypothesis that HBO₂ increases PO₂ in brain in direct proportion to rCBF.