Regional cerebral blood flow and glucose utilization during hypoglycemia in newborn dogs

To assess alterations in regional cerebral blood flow and glucose utilization during perinatal hypoglycemia, newborn dogs (2-7 days postnatal age) were anesthetized with halothane, tracheostomized, paralyzed, and artificially ventilated with 70% N₂O-30% O₂ to maintain arterial normoxia and normocapnia (arterial PO₂>60 mmHg; arterial PCO₂: 35-42 mmHg; arterial pH: 7.35-7.45). Regional cerebral blood flow (rCBF) and glucose utilization (rCGU) were determined with iodo-[¹⁴C]antipyrine and 2-deoxy-[¹⁴C]glucose as the radioactive tracers, respectively. Hypoglycemia with blood glucose concentrations averaging 0.9 mmol/l was achieved within 90-120 min in 10 animals using intermittent intravenous injections of regular insulin; 10 control animals received 0.9% saline (blood glucose = 9 mmol/l). During hypoglycemia, mean arterial blood pressure was 81% of control, whereas heart rate was unchanged. Arterial O₂ and acid-base balance were well maintained (arterial PO₂ = 68 mmHg; PCO₂ = 37 mmHg; pH = 7.35). Hypoglycemia was associated with significant increases in rCBF in all of 16 analyzed structures, ranging from 172% (parietal white matter) to 249% (thalamus) of control values (17-65 ml·100 g^-1·min^-1). During hypoglycemia, rCGU was relatively unchanged from normoglycemic values in 11 of 16 brain structures. Significant reductions in rCGU were seen only in occipital white matter -31%) and in the cerebellar vermis and hemisphere (-31 and -43%, respectively). CGU actually increased slightly in the pons and medulla (+12 and +19%, respectively). Calculation of the extent to which glucose transport into brain during hypoglycemia was enhanced by the increase in CBF suggested that glucose delivery (CBF x blood glucose concentration) contributed little (<10%) to the maintenance of CGU. Presumably, other factors, notably low cerebral energy demands, serve to maintain cerebral glucose homeostasis of the immature brain during hypoglycemia.