Free Fatty Acids and Energy Metabolites in Ischemic Cerebral Cortex with Noradrenaline Depletion

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Abstract
Cerebral noradrenaline [norepinephrine] (NA) may play a central role in mediating the increased production of free fatty acids (FFA) during cerebral ischemia. Levels of FFA, cAMP and NA, as well as ATP, ADP and AMP, were measured in cerebral cortex during decapitation ischemia in rats 2 wk after unilateral locus ceruleus lesion. Comparisons were made between the results obtained from the contralateral cortex with normal NA content and the NA-depleted ipsilateral cortex. Although NA depletion was associated with a diminished transient rise of cAMP in response to ischemia, it failed to influence the magnitude of FFA increase or the decline of energy state within the 15-min period of ischemia. A more than 2-fold increase of total FFA (sum of palmitic, stearic, oleic, arachidonic and docosahexaenoic acids) was observed in both hemispheres at 1 min after decapitation, when energy failure became manifest. The increased production of FFA continued throughout the 15 min of ischemia, with a preferential rise in the levels of stearic and arachidonic acids. There was an inverse correlation between FFA levels and total adenylate pool. The results do not support a major role for NA and cAMP in increasing cortical FFA during complete ischemia. They are consistent with the view that impaired oxidative phosphorylation activates deacylating enzymes. Disturbance of reacylation due to energy depletion is probably another factor contributing to the continuous increase of FFA during prolonged ischemia.