This study examined the effects of
hypoglycemia (HG) on cerebral metabolism and cerebrovascular reactivity to
carbon dioxide. Cerebral blood flow (CBF) was determined using radiolabeled
microspheres in
pentobarbital-anesthetized dogs. Cerebral
oxygen,
glucose,
lactate,
pyruvate,
acetoacetate, and
beta-hydroxybutyrate uptakes were calculated using the respective concentrations measured in arterial and sagittal sinus blood samples. EEG was recorded throughout each experiment. HG was induced with
insulin to obtain a
blood glucose less than 30 mg/100 ml.
Hypercapnia was studied in 10 animals (3 control, 7 HG) by increasing arterial
carbon dioxide tension (PaCO2) from control (35 +/- 4; mean +/- SE) to 54 +/- 2 Torr during normoglycemia (NG) and HG.
Hypocapnia was studied in 11 animals (3 control, 8 HG) by decreasing PaCO2 from control (39 +/- 1) to 14 +/- 1 Torr in NG and HG. Measurements were taken after reaching steady-state PaCO2 in both groups at each control and altered PaCO2 state. In the hypercapnic group,
glucose decreased from 71 +/- 3 to 28 +/- 3 mg/100 ml. CBF increased with
hypercapnia to 175% of control in both NG and HG. Cerebral metabolic rate of
oxygen and electroencephalogram (EEG) did not change in the hypercapnic group. In the hypocapnic group
glucose decreased from 71 +/- 3 to 19 +/- 2 mg/100 ml. CBF decreased with
hypocapnia to 62 +/- 5% of control in NG but remained at control in HG. This was not accompanied by changes in cerebral oxygen consumption; however, a flat EEG occurred in all HG hypocapnic animals. No change occurred in uptake of the other cerebral metabolites measured in any group. This study shows that the CBF hypercapnic response remains intact during HG; however,
hypocapnia causes severe EEG disturbances and impairs the cerebral vasoconstriction response.