Cerebrovascular and metabolic responses to hypoxia during hypoglycemia in dogs

The effects of insulin-induced hypoglycemia on the response of cerebral blood flow (CBF-microspheres), electroencephalogram (EEG), and cerebral uptake/production of oxygen (CMRO₂), glucose (CMRglu), lactate, pyruvate, β-hydroxybutyrate, and acetoacetate to isocapnic hypoxic hypoxia were studied in pentobarbital-anesthetized, mechanically ventilated dogs. Hypoglycemia [1.3 ± 0.2 μmol/ml, ±SE); n = 9] did not produce an isoelectric EEG and did not affect base-line CBF or CMRO₂. When arterial O₂ content was reduced from 17.4 ± 0.6 to 7.5 ± 0.5 and 5.1 ± 0.2 vol% during hypoglycemia, CBF increased from 25 ± 3 to 54 ± 6 and 84 ± 8 ml·100g^-1·min^-1, respectively. This response was not different from that during normoglycemia (3.5 ± 0.3 μmol/ml; n = 12). During normoglycemia, hypoxia increased CMRglu from 17.0 ± 1.2 to 32.2 ± 4.7 and 49.9 ± 6.6 μmol·100 g^-1·min^-1, respectively. Hypoglycemia did not affect CMRglu during normoxia, but the hypoxia-induced increase in CMRglu was abolished. CMRO₂ during hypoxia was unaffected by hypoglycemia. We conclude that levels of hypoglycemia that do not produce an isoelectric EEG may impair the normal increase in CMRglu during hypoxia but do not alter the global CBF response to hypoxia.