Dexamethasone and local cerebral glucose utilization in freeze‐traumatized rat brain

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Abstract
Local cerebral glucose utilization (LCGU) was studied using the 14C-deoxyglucose method in dexamethasonetreated rats with focal cortical freezing lesions. Widespread depression of LCGU, which developed with time after the lesion in untreated animals, was significantly diminished by dexamethasone (0.25 mg/kg/day) started either 6 to 18 hours before or 4 or 24 hours after the lesion. The effect of dexamethasone was most striking in cortical areas of the traumatized hemisphere, where the depression was most profound in untreated animals. Thus, three days after the lesion, average LCGU in these regions was 47% and 72% of normal in untreated and pretreated rats, respectively. Dexamethasone also affected LCGU bilaterally in subcortical structures and in white matter. The results suggest that dexamethasone modified the widespread depression in functional state of the rat brain that developed in response to injury. Since the spatial distribution and time course of the observed changes in LCGU did not parallel those of cerebral edema, these effects of dexamethasone do not appear to be mediated by effects on the edematous process.