Influence of CO2 on Cerebral O2 Metabolism During Sustained Hypoxia

Zachary M. Smith¹, Ethan Li¹, David J. Dubowitz¹

Hypobaric hypoxia is accompanied by an increase in cerebral O₂ metabolism. During acute hypoxia this CMRO₂ rise can be paritally mitigated by maintaining arterial CO₂ at its normoxic level. We investigated if acetazolamide (a carbonic anhydrase inhibitor that increases CO₂ in the cerebral tissues) modulated this CMRO₂ increase during sustained hypoxia. CMRO₂ was measured using ASL and TRUST at 3T in human volunteers during normoxia, and following 2-days sustained hypoxia with or without treatment with acetazolamide. Following acetazolamide, the hypoxia-induced rise in CMRO₂ was reduced. These data provide evidence for a CO₂ dependence of the CMRO₂ rise during sustained hypobaric hypoxia.