Abstract #0948

Bartnik B, Sutton R, Hovda D

Traumatic brain injury is associated with metabolic alterations that may contribute to energy crisis. The present study was designed to explore the metabolic fate of [1, 2 13C2] glucose in the rat cortex 3.5h and 24h after a fluid percussion injury, where we have previously established a period of immediate hyperglycolysis followed by a decrease in ATP synthesis and a period of metabolic depression. Our results show an injury induced decrease in glucose utilization and subsequent glutamate and glutamine isotopomer labeling. Increased metabolism through the pentose phosphate and pyruvate recycling pathways suggest an increased need for reducing equivalents after injury.