The effects of hypoglycaemia on cerebral blood flow and metabolism in the new‐born calf.

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Abstract
The effects of insulin hypoglycemia on cerebral blood flow and metabolism were examined in unanesthetized, unrestrained calves between 1-26 days after birth. Cerebral blood flow was measured with an inert gas technique using molecular H and cerebral metabolism was quantified by determination of arteriocerebral venous (A-V) concentration differences for O2, glucose, lactate, pyruvate, acetoacetate, .beta.-D-hydroxybutyrate and ammonia. During normoglycemia the mean (A-V) difference for glucose was close to 1/6 that of O2 on a molar basis. A small net loss of pyruvate from the brain was found but there was no significant (A-V) difference for lactate. Arterial concentrations of acetoacetate and .beta.-D-hydroxybutyrate were low and no utilization of ketone bodies by the brain was demonstrated. Moderate hypoglycemia (arterial plasma glucose concentration 1-2 mmol/l) had no measurable effect on cerebral blood flow or metabolism. During profound hypoglycemia (arterial plasma glucose concentration < 1.0 mmol/l) cerebral glucose uptake was sufficient to account for 56% of the cerebral O2 consumption. Cerebral O2 consumption fell in comatose animals but increased during hypoglycemic convulsions as did cerebral blood flow. In day-old calves hypoglycemia was associated with a rise in blood lactate concentration and uptake of lactate by the brain. A net loss of ammonia by the brain was observed during hypoglycemia in calves at all ages examined. The loss was greater in convulsing than in comatose animals.