The increase in local cerebral glucose utilization following fluid percussion brain injury is prevented with kynurenic acid and is associated with an increase in calcium.

Immediately following a lateral fluid percussion brain injury, the cerebral cortex and hippocampus ipsilateral to the percussion show a marked accumulation of calcium and a pronounced increase in glucose metabolism. To determine if this increase in glucose metabolism was related to the indiscriminate release of the excitatory amino acid (EAA) glutamate, kynurenic acid (an EAA antagonist) was perfused into the cerebral cortex through a microdialysis probe for 30 min prior to injury. The results show that adding kynurenic acid to the extracellular space prior to trauma prevents the injury-induced increase in glucose utilization. These results indicate that calcium contributes to the ionic fluxes that are typically seen following brain injury and supports the concept of an increased energy demand upon cells to drive pumping mechanisms in order to restore membrane ionic balance.