Hypermetabolic state following experimental head injury

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Abstract
Results were as follows: (I) i) Glucose uptake was reduced at the center of the contusion in all cases. ii) Two different effects were observed in LCGU change two hours after injury: normal or slight increase in four of six rats (type A) and a remarkable increase in the cortex of the injured hemisphere in two of six rats (type B). iii) The pattern of increase in LCGU (type B) resembles that of cortical spreading depression. (II) i) Negative shift of DC-potential concomitant with EEG suppression in the injured hemisphere was observed frequently one to two hours after injury. ii) The increased LCGU pattern during DC-potential negative shift was identical with that of type B. iii) LCGU pattern without DC-potential change resembles that of type A. We concluded that the hypermetabolism occurring in the damaged cortex was due to a spreading depression. The findings obtained here should yield very important information concerning pathogenesis and treatment of human head injury.