We previously reported that intravenous (i.v.) administration of large volumes (0.2 ml/g) of either an isotonic dextrose-free solution or 5% dextrose solution given over 18 h after closed head trauma (CHT) in rats did not significantly affect neurological severity score or brain tissue specific gravity. However, it is possible that with more rapid administration, isotonic or 5% dextrose i.v. solutions may alter neurological outcome after CHT. Our study examined whether neurological severity score, brain tissue specific gravity and water content, and blood compostition were significantly altered when 0.25 ml/g of either 0.9% saline or 5% dextrose was given i.v. over 0.5 h (rather than over 18 h) after CHT. Eighty-four rats that survived ether anesthesia and CHT were randomly assigned to one of 11 experimental groups. Saline- and dextrose-treated rats were evaluated at 4 and 48 h after CHT and were compared to rats without CHT and to untreated rats at 4 and 48 h after CHT. There were no statistically significant differences in neurologic outcome and brain edema between the untreated and the saline-treated groups. However, 5% dextrose i.v. increased mortality (group 6 and 11, 50 and 0% survivors, respectively), decreased specific gravity in the noncontused hemisphere, and worsened neurologic outcome with and without CHT. Blood osmolality remained stable in comparison to the baseline value of 291.9 ± 7.4 mOsm/kg (mean ± SD). Sodium and glucose levels, initially 139.2 ± 2.6 mEq/L and 168 ± 61.9 g%, remained stable in the saline-treated animals at 138 ±2.1 mEq/L and 162.7 ± 18.5 g%, but after 5% dextrose i.v. administration, values decreased to 86.3 ± 9.7 mEq/L and increased to >450 mg/dl, respectively. We conclude that in our model of CHT, giving large boluses of 0.9% saline i.v. does not affect electrolyte balance, neurologic outcome, or formation of brain edema in rats with or without CHT. However, the same volume of 5% dextrose i.v. decreased serum sodium, increased brain edema in the noncontused hemisphere (in rats with CHT) and in intact brains (in rats without CHT), and decreased neurological outcome with and without CHT.