REGIONAL ACTIVITY OF ORNITHINE DECARBOXYLASE AND EDEMA FORMATION AFTER TRAUMATIC BRAIN INJURY

THIS STUDY EXAMINED ornithine decarboxylase (ODC) activity and edema f ormation bilaterally in brain cortices and hippocampi after lateral co ntrolled cortical-impact injury in rats. To measure the activity of OD C, the brains of injured and control rats were frozen in situ at 30 mi nutes and at 6, 24, and 72 hours after controlled cortical-impact inju ry of moderate severity. The specific gravity of these regions was exa mined in decapitated animals at corresponding time points as an indica tor of edema formation. Thirty minutes after injury, ODC activity did not increase in the injury-site cortex and ipsilateral hippocampus. At 6 hours after injury, ODC activity had increased by nine times that o f the control in the injury-site cortex, by five times in the adjacent cortex, and by five and one-half times in the ipsilateral hippocampus . Twenty-four hours after injury, ODC activity had increased by three times that of the control in the injury-site cortex and two times in t he ipsilateral hippocampus. Seventy-two hours after injury, activity h ad returned to control levels. ODC activity increased significantly in the contralateral cortex and hippocampus only at 6 and 24 hours. The injury-site and adjacent cortices and the ipsilateral hippocampus show ed significant edema at 6, 24, and 72 hours but not at 30 minutes afte r injury. These findings indicate that polyamine metabolism is signifi cantly altered in traumatic brain injury. The temporal association bet ween ODC activity and edema formation indicates that polyamines might be a contributing factor in edema formation after traumatic brain inju ry. The delayed induction of ODC after brain injury suggests a potenti al therapeutic window for future pharmacological intervention to decre ase posttraumatic secondary cerebral injury.