Abstract
To determine whether lactic acid is a cerebral substrate during and after partial ischemia in piglets, cerebral blood flow and arteriovenous differences of O2 and substrates were measured during control, after hemorrhagic hypotension, and 10 and 90 minutes after reperfusion with blood. During and following ischemia, alterations in cerebral O2 and glucose uptake indicated disturbed oxidative metabolism. Cerebral lactic acid uptake was similar at control, hypotension, and 90 minutes postreperfusion, but rose 10 minutes postreperfusion. Absent cerebral production of lactic acid during and net uptake following ischemia do not support lactic acid as a substrate since insufficient O2 was available for oxidation.
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