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 increased 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/reperfusion-evoked release of amino acids from the rat
cerebral cortex. Physiologic levels of glucose significantly reduced the amount of
aspartate, glutamate and γ-aminobutyric acid and the supra-physiologic levels of glucose
reduced the amount of aspartate and phosphoethanolamine released from the cortex during
ischemia/reperfusion in comparison with no glucose. The decrease 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 may also reflect the continued energy-dependent uptake
of glutamate by glial cells.
Key words
Glutamate - Aspartate - Hyperglycemia - Cerebral Ischemia - Reperfusion