Lactate Uptake and Metabolism by Brain During Hyperlactatemia and Hypoglycemia

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Abstract
Entry into CSF and consumption by brain of blood-borne lactate (La) was quantified in pentobarbital-anesthetized, normocapnic dogs loaded and infused with NaLa and HLa to hold constant, in arterial blood, both the La concentration at about 8 mM (normal = 1 mM) and the pH at 7.4. In four dogs studied hourly over six hours, the arteriosagittal sinus blood concentration difference (δA-V La) was 0.41 ± 0.14 (SE) mM (P 2 were determined at 30-minute intervals. CBF and cerebral metabolic rate of O2 (CMRO2) both fell about 17% during two hours of hypoglycemia and returned to control with La loading although blood glucose continued to fall to 1.5 mM. In the two hour La loaded period δA-V La was 0.27 ± 0.10 mM (n = 32) and CSF La rose to 0.7 of arterial La without altering CSF pH. CMRO2 averaged 1.61 ± 0.14 µ mol/(min.gm brain), of which CMR glucose (x6 to give O2, equivalents) provided 75% or 1.18 ± 0.13 µ O2 eq/(min.gm). CMR La x 3 was 28% of CMRO2 or 0.45 ± 0.15 µ eq/(min.gm). The results suggest that blood-borne La can stoichiometrically replace about one-fourth of the glucose used as brain substrate during hypoglycemia, and probably during normoglycemia. Uptake may be limited by saturation of carriers facilitating passage of La across the blood-brain barrier and into brain cells.