Demonstration of hyperaccumulation of [18F]2-fluoro-2-deoxy-D-glucose under oxygen deprivation in living brain slices using bioradiography

To clarify the mechanism of hyperaccumulation of glucose in acute brain ischemia by PET, changes of glucose metabolism and mitochondrial electron transfer function were examined in living brain slices in vitro during control, hypoxic, and anoxic conditions by positron autoradiography using [F-18]2-fluoro-2-deoxy-D-glucose ([F-18]FDG) and [O-15]oxygen. [O-15]Oxygen fixation reflecting mitochondrial electron transfer function was reduced and [F-18]FDG uptake reflecting glucose metabolism was increased in proportion to the strength of oxygen deprivation during anoxia and hypoxia. Mitochondrial electron transfer function decreased with no regional differences, whereas the glucose metabolism was the most enhanced in the hippocampus and thalamus. The enhanced glucose metabolism was associated with an increased glutamate efflux after hypoxia and anoxia. Glucose metabolism was also increased by the addition of glutamate and was attenuated by the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 in the hippocampus and thalamus. The hyperaccumulation of glucose in acute brain ischemia was demonstrated in living brain slices using bioradiography with reduced mitochondrial electron transfer. The activation of NMDA receptors by glutamate during acute brain ischemia might be responsible for hyperutilization of glucose in the hippocampus and thalamus. (C) 2005 Wiley-Liss, Inc.