Zachary M. Smith1, Ethan Li1, David J. Dubowitz1
1Center for Functional MRI, University of California San Diego, La Jolla, CA, United States
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.