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Summary: Immediately following concussive brain in jury, cells exhibit an increase of energy demand repre sented by the activation of glucose utilization. We have proposed that this trauma-induced hypermetabolism re flects the effort of cells to restore normal ionic balance disrupted by massive ionic fluxes through transmitter gated ion channels. In the present study, changes in local CMR g lc following fluid-percussion concussive injury were determined using [14C]2-deoxy-n-glucose autoradi ography, and the effects of in situ administration (via mi crodialysis) of excitatory amino acid (EAA) antagonists [kynurenic acid (KYN), 2-amino-5-phosphonovaleric acid (APV; 100 fJ,M, I mM, and 10 mM), and 6-cyano-7-nitroquinoxaline-2,3-dine (CNQX; 300 fJ,M, I mM, and 10 mM] on glucose utilization were investigated. Animals that did not receive dialysis showed a remarkable inIn recent work using microdialysis, the changes in extracellular potassium ([K + ] e ) and the release of excitatory amino acids (EAAs) have been docu mented following experimental concussive (Katayama et aI. , 1988(Katayama et aI. , , 1990) and contusion (Faden et aI., 1989; Nilsson et aI. , 1990) brain injury. InRe

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Intravascular volume expansion in the presence of excessive natriuresis requires a large sodium and water intake and is often associated with hyponatremia. Inhibition of natriuresis with fludrocortisone can effectively reduce the sodium and water intake required for hypervolemia and prevent hyponatremia at the same time.

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