Vink R, Golding E M, Headrick J P
Division of Biochemistry and Human Physiology, James Cook University of North Queensland, Townsville, Australia.
J Neurotrauma. 1994 Jun;11(3):265-74. doi: 10.1089/neu.1994.11.265.
Studies of fluid percussion-induced traumatic brain injury have shown that moderate trauma results in ionic imbalances, with resultant increases in energy demand to restore these ion gradients. Because there are also increased rates of glucose metabolism during periods of focal decline in blood flow, it has been suggested that the mitochondria may be incapable of sufficient oxidative metabolism to cope with this increased energy demand after injury and that ATP derived from substrate level phosphorylation must meet this demand. In the present study, we used phosphorus magnetic resonance spectroscopy to determine the mitochondrial capacity for oxidative phosphorylation after moderate brain trauma. Before injury, mean oxidative capacity was 54% +/- 1%. After injury, mean capacity increased significantly (p < 0.001) to a maximum of 61% +/- 1%, indicating that mitochondrial oxidative metabolism was enhanced after trauma. Increased oxidative capacity was accompanied by increases in ADP, AMP, and inorganic phosphate concentrations and was correlated to decreases in cytosolic phosphorylation ratio. We conclude that moderate brain trauma increases mitochondrial rate of ATP synthesis over the first 4 h posttrauma, and that during this time of increased ATP turnover, positive feedback regulation of glycolysis by increased concentrations of ADP, AMP, and inorganic phosphate contributes to maintenance of metabolic steady state.
