Regional Cerebral Glucose Utilization Transiently Increases during Mild Hypoxia

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Abstract
Regional cerebral glucose utilization (rCMRglu) 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 CMRglu 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 CMRglu was measured in 17 brain regions using [6-14C]glucose. Pao2 decreased from 88 mm Hg in the controls to ∼40 mm Hg during hypoxia. In the early stages of hypoxia (2–12 min), rCMRglu increased ∼10–25% above the control rates. In later stages of hypoxia (17–27 min), rCMRglu was not different from that in the normoxic controls. The increase in rCMRglu 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 rCMRglu. 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.