• Fredrik Clausen, Lars Hillered, and Jan Gustafsson.
• Department of Neuroscience, Neurosurgery, Uppsala University, Entrance 85, 2nd floor, Uppsala University Hospital, 751 85, Uppsala, Sweden. fredrik.clausen@neuro.uu.se
• Acta Neurochir (Wien). 2011 Mar 1;153(3):653-8.

BackgroundFollowing traumatic brain injury (TBI), a disturbed cerebral glucose metabolism contributes to secondary brain damage. To study local cerebral glucose metabolism after TBI, we delivered (13)C-labeled glucose into brain tissue by microdialysis (MD).MethodMD probes were inserted bilaterally into the parietal cortex of rat brain, one probe in the shear stress zone of the injury and the other at the corresponding contralateral coordinates. A moderately severe controlled cortical contusion was used to model TBI. Dialysate concentrations of glucose, pyruvate, lactate, and glycerol were measured, and following derivatization, (13)C enrichments of the compounds were determined by gas chromatography-mass spectrometry.FindingsWe found that (13)C-labeled glucose was rapidly converted into (13)C-lactate and (13)C-glycerol. In the hours following TBI, concentrations and (13)C enrichments of lactate and glycerol increased.ConclusionsThe findings confirm the occurrence of anaerobic local glucose metabolism early after TBI. Only a small fraction of the glycerol was newly synthesized, suggesting that the hypothesis that most of the released glycerol after TBI comes from degradation of membrane phospholipids still holds. We conclude that the combination of microdialysis and stable isotope technique is a useful tool for investigating local glucose metabolism following brain injury.

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