Rapid Efflux of Lactate from Cerebral Cortex during K+-Induced Spreading Cortical Depression

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Abstract
Rapid transport of lactate from activated brain regions to blood, perhaps reflecting enhanced metabolite trafficking, would prevent local trapping of labeled metabolites of [6-14C]glucose and cause underestimation of calculated CMRglc. Because the identities of glucose metabolites lost from activated structures and major routes of their removal are not known, arteriovenous differences across brains of conscious normoxic rats for derivatives of [6-14C]glucose were determined under steady-state conditions in blood during K+-induced spreading cortical depression. Lactate was identified as the major labeled product lost from brain. Its entry to blood was detected within 2 minutes after a pulse of [6-14C]glucose, and it accounted for 96% of the 14C lost from brain within approximately 8 minutes. Lactate efflux corresponded to 20% of glucose influx, but accounted for only half the magnitude of underestimation of CMRglc when [14C]glucose is the tracer, suggesting extensive [14C]lactate trafficking within brain. [14C]Lactate spreading within brain is consistent with (1) relatively uniform pattern labeling of K+-treated cerebral cortex by [6-14C]glucose contrasting heterogeneous labeling by [14C]deoxyglucose, and (2) transport of 14C-labeled lactate and inulin up to 1.5 and 2.4 mm, respectively, within 10 minutes. Thus, newly synthesized lactate exported from activated cells rapidly flows to blood and probably other brain structures.