Regional brain glucose utilization in the conscious rat exposed to prolonged hypobaric hypoxia

Because of the physiologic and metabolic changes that occur during acclimatization, we hypothesized that LCGU may be normal during prolonged hypoxia. We exposed five Sprague-Dawley rats to hypoxia (air at 380 mm Hg) for 2 weeks (hypoxic group) and six rats to 2 weeks of hypoxia followed by 2 weeks of recovery in room air (recovered group). Six control rats breathed room air (control group). Regional brain glucose utilization was measured in awake animals by using 2-[C]deoxyglucose autoradiography. Glucose utilization was comparable in the control and recovered groups and in most brain regions of hypoxic animals. Glucose utilization was decreased slightly in 10 of 12 gray matter regions examined and was 20 to 25% lower (p <0.05) in the olfactory and auditory cortices, the caudate nucleus, and the superior olive of the hypoxic group. White matter glucose utilization was unchanged. Hypoxic rats, compared to controls, had a lower PaO2 (53 +/- 3 vs. 76 +/- 3 mm Hg, mean SEM, respectively), a lower PaCO2 (22 +/- 1 vs. 36 +/- 2 mm Hg), and a higher mean pulmonary artery pressure (46 +/- 3 vs. 14 +/- 3 mm Hg) and hematocrit (61 +/- 2% vs. 48 +/- 1%; p <0.005 for all comparisons). Pulmonary hypertension and polycythemia persisted in recovered rats. Arterial pressure, pH, and plasma glucose were unaffected. Therefore, while acute hypoxia may increase glucose utilization in most brain structures, prolonged exposure does not.