Regional cerebral glucose utilization transiently increases during mild hypoxia

Regional cerebral glucose utilization (rCMR(glu)) was studied during mild hypoxic hypoxia in awake free-ranging rats. Rats were prepared with chronic arterial and venous catheters and placed in individual chambers for 4 days to recover from surgery before the experiments. The catheters were accessible by passing them through the top of the chambers. Hypoxia was induced by filling the chambers with a gas mixture consisting of 11% O₂ in a balance of N₂. Regional CMR(glu) and physiological parameters were measured in normoxic controls and in rats that had been hypoxic for 2 and 17 min before beginning the measurements. Regional CMR(glu) was measured in 17 brain regions using [6-¹⁴C]glucose. P(a)O₂ decreased from 88 mm Hg in the controls to ~ 40 mm Hg during hypoxia. In the early stages of hypoxia (2-12 min), rCMR(glu) increased ~ 10-25% above the control rates. In later stages of hypoxia (17-27 min), rCMR(glu) was not different from that in the normoxic controls. The increase in rCMR(glu) in the early hypoxia was not blocked by propranolol (1.4 mg/kg), indicating that beta-adrenergic receptors were not involved with the increase in rCMR(glu). It was concluded that mild hypoxia is associated with an increased rate of cerebral glucose utilization; however, the increase is transitory, with glucose utilization returning to control rates before 17 min.