Cerebral Blood Flow and Metabolism During Hypoglycemia in Newborn Dogs

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Abstract
Cerebral blood flow (CBF) and cerebral metabolic rates (CMR) were studied in newborn dogs during insulin-induced hypoglycemia. Pups were anesthetized, paralyzed and artificially ventilated with a mixture of 70% nitrous oxide and 30% O2 to maintain normoxia and normocarbia. Experimental animals were given regular insulin (0.3 units/g i.v.); controls received normal saline. CBF was determined using a modification of the Kety-Schmidt technique using 133Xe as indicator. Arteriovenous differences for O2, glucose, lactate and .beta.-hydroxybutyrate (.beta.-OHB) were measured and CMRO2 and CMRsubstrates calculated. Two groups of hypoglycemic dogs were identified; those in which blood glucose levels were > 0.5 mM (group 1) and those in which they were < 0.5 mM (group 2). CBF did not change significantly from control values of 23 .+-. 10 ml/min per 100 g (mean .+-. SD) at both levels of hypoglycemia. Hypoglycemia did not alter CMRO2 significantly from its initial level of 1.05 .+-. 0.37 ml O2/min per 100 g. Glucose consumption in brain during normoglycemia accounted for 95% of cerebral energy supply, with minimal contributions from lactate (4%) and .beta.-OHB (0.5%). During hypoglycemia, CMRglucose declined by 29 and 52% in groups 1 and 2, respectively; CMRlactate increased and became the dominant fuel for oxidative metabolism in brain. The cerebral utilization of .beta.-OHB was unaltered by hypoglycemia. Insulin-induced hypoglycemia in the newborn dog is associated with an increase in cerebral lactate utilization, supplementing glucose as the primary energy fuel and preserving a normal CMRO2. These metabolic responses may contribute to the tolerance of the immature nervous system to the known deleterious effects of hypoglycemia.