Lactate uptake and metabolism by brain during hyperlactatemia and hypoglycemia.

Lactale Uptake and Metabolism by Brain During Hyperlactatemia and Hypoglycemia • 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 (AA-V La) was 0.41 ± 0.14 (SE) mM (P < 0.05) and was time independent. CSF La rose slowly over four hours to about 0.6 of blood La while cisternal CSF pH remained nearly constant. Four acetate loaded controls showed no changes of AA-V La, CSF La, CSF, or arterial pH. Brain uptake of La was quantitated in eight dogs during insulin-induced hypoglycemia, to minimize possible competition by glucose. Cerebral blood flow (CBF) and AA-V for La, glucose, and O, were determined at 30-minute intervals. CBF and cerebral metabolic rate of O, (CMROi) 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 AA-V La was 0.27 ± 0.10 mM (n = 32) and CSF La rose to 0.7 of arterial La without altering CSF pH. CMRO, averaged 1.61 ± 0.14 n mol/(min-gm brain), of which CMR glucose (X6 to give O, equivalents) provided 75% or 1.18 ±0.13 fi O, eq/(min-gm). CMR La X 3 was 28% of CMRO, or 0.45 ± 0.15 y. O, 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. Additional