Abstract
The changes in local cerebral glucose utilization (LCGU) following a fluid-percussion injury were studied in 23 rats using the 2-deoxyglucose (2-DG) technique in order to determine the critical period for neuronal damage.
Three rats were used as controls. All the rats received a moderate impact of 4.8-5.6 atm from a fluidpercussion device using the University of California, San Francisco, method. LCGU was studied at 15, 30, 45, 60, and 120 min and 24 hours after injury. The optical density on autoradiographs was measured at the site of the brain contusion, in the rim around the contused brain, and in the bilateral cerebral cortex, hippocampus, and thalamus.
Decreased 2-DG uptake was observed in the contused brain. However, increased 2-DG uptake was seen in the rim around the contused brain from 15-60 min after injury.
The changes in 2-DG uptake noted in this study were very similar to those caused by permanent focal ischemia in a previous study, which suggests that the pathophysiologic phenomena occurring after fluidpercussion injury in the rat brain are based on ischemic changes.
