CEREBRAL EXTRACELLULAR GLUCOSE AND LACTATE CONCENTRATIONS DURING AND AFTER MODERATE HYPOXIA IN GLUCOSE-INFUSED AND SALINE-INFUSED RATS

To assess the effect of a glucose infusion on brain extracellular fluid (ECF) during systemic hypoxia, changes in glucose and lactate concentrations in cerebral ECF during and after moderate hypoxic hypoxia were measured in adult, conscious, unrestrained rats, with a microdialysis probe in the posterior hippocampus. The rats were given either saline (n = 6) or 50% glucose solution (n = 6) for 3 h, starting 60 min before the onset of hypoxia. Hypoxia was produced by circulating 7% O2 gas in a plastic chamber for 90 min. In saline-infused animals, brain ECF glucose concentrations decreased slightly during hypoxia, although blood glucose concentrations did not change. Blood lactate concentrations increased to 6.28 +/- 0.91 mM, at 60 min after the onset of hypoxia (P < 0.05). Brain ECF lactate concentrations increased to 3.53 +/- 0.20 mm and remained constant during 60 min of steady-state hypoxia (P < 0.05) and decreased to the basal level within 60 min after the end of hypoxia. When sodium lactate solution was infused intravenously for 90 min (n = 4), blood lactate concentrations increased to a level as high as those found during hypoxia. However, the brain ECF lactate concentration increased only to 1.86 +/- 0.09 mM. In glucose-infused animals, the blood glucose concentration reached 339.1 +/- 32.3 mg/dl at the end of the glucose infusion, and the brain ECF glucose concentration increased to 54.7 +/- 7.3 mg/dl. Although the blood lactate concentration during hypoxia was significantly higher in the glucose-infused group than in the saline-infused group, there was no significant difference in the brain ECF lactate concentrations between these groups. In conclusion, the current study suggests that glucose supply is not a rate-limiting factor for anaerobic glycolysis in the brain, and the lactate produced in brain tissue seems to be used within the brain during and after a period of moderate hypoxia.