Alterations in cerebral energy metabolism induced by traumatic brain injury

Energy metabolism of the brain is unique, possessing high aerobic metabolis m with no significant capacity for anaerobic glycolysis and limited tissue stores of glucose. A steady supply of oxygen and glucose is essential in or der to maintain cerebral function and integrity. Extensive research in expe rimental and human head injury has been conducted regarding the delivery of oxygen and outcome. This research has provided evidence which indicates th at in addition to the availability of oxygen and glucose, other factors, su ch as perturbation of mitochondrial energy transducing processes which also follow head trauma, play significant roles. In this paper, the salient fin dings from biochemical studies of experimental and clinical brain injury ar e summarized and indicate that the mitochondrial respiratory chain-linked o xidative phosphorylation and calcium transport are compromised by trauma-in duced brain injury and support the idea that oxidative stress and perturbat ion of cellular calcium homeostasis play significant roles in traumatic bra in injury.