Topical glucose and accumulation of excitotoxic and other amino acids in ischemic cerebral cortex

Pre-ischemic hyperglycemia aggravates brain damage due to transient global ischemia as demonstrated by exacerbation of brain lesions. Lactacidosis and elevated glutamate levels have been implicated as mechanisms of the increa sed damage. Our objective was to determine the effects of different levels of glucose (0, 66.5, 450 mg/dL) in cortical superfusates on the ischemia/re perfusion-evoked release of amino acids from the rat cerebral cortex. Physi ologic levels of glucose significantly reduced the amount of aspartate, glu tamate and gamma-aminobutyric acid and the supra-physiologic levels of gluc ose reduced the amount of aspartate and phosphoethanolamine released from t he cortex during ischemia/reperfusion in comparison with no glucose. The de crease in glutamate release may be due to increased availability of glucose for glycolysis with the subsequent formation of ATP and lactate, which has been shown to act as an energy source for neurons. The decreased levels ma y also reflect the continued energy-dependent uptake of glutamate by glial cells.