[Glucose metabolism in trauma-induced brain edema, with special reference to local blood circulation and blood-brain barrier].

Local cerebral glucose utilization (LCGU) was studied using the carbon 14-deoxyglucose method in rats with local freezing lesion in the left parietal cortex. A depression of LCGU developed with time after the lesion, being most prominent throughout the cortical areas of the lesioned hemisphere 3 days after lesion. Corresponding results in other regions were contralateral cortical areas, ipsilateral and contralateral subcortical structures. Brain stem structures were not affected. In white matter bilateral depression of LCGU reached its peak 24 hours after the lesion. LCGU returned to normal within 5 days in all affected areas. The areas affected and the time-course of the observed changes did not correlate with the location and known time-course of development of cerebral edema. Local cerebral blood flow (LCBF) was measured 1 and 3 days after a freezing lesion using the carbon 14-iodoantipyrine method. Twenty-four hours after a freezing lesion normal LCBF were seen throughout the traumatized brain. Three days after the lesion an increased LCBF involved all cortical areas, with the hyperemia being more pronounced in the hemisphere contralateral to the lesion. No corresponding changes in LCBF were observed. Evans blue dye was injected intravenously before the start of the barrier (BBB) at each time period following the lesion could be determined. Blue staining was seen in the area of the lesion in all animals killed 4 or 24 hrs after the lesion was made, indicating a BBB permeable to the Evans blue-serum protein complex.(ABSTRACT TRUNCATED AT 250 WORDS)