A BS T R A C T After the intraperitoneal injection into young mice of 700-800 mg/kg of salicylate, brain glucose fell to one-third or less of control values despite normal plasma glucose levels; brain lactate was nearly doubled and there were small decreases in phosphocreatine (18%) and in glycogen (17%). ATP, pyruvate, a-ketoglutarate, and glutamate were unchanged. In liver, glycogen was reduced 79% and lactate was five times higher than in control animals; glucose, glucose-6-phosphate, and ATP were unchanged.Since salicylate uncouples oxidative phosphorylation, it is postulated that high energy phosphate in the brain is maintained near normal levels by a compensatory increase in cerebral glycolysis. Apparently the brain glucose level falls because the rate of utilization exceeds the rate at which glucose can be supplied from the blood. Concurrent administration of glucose with salicylate elevated brain glucose concentration and was associated with striking improvement in the condition and the increased survival of the animals. These findings stress the fact that in salicylate poisoning the supply of glucose to the brain may be inadequate even when blood glucose levels are normal.

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—Fructose levels were determined in plasma and brain of 8‐ to 12‐day‐old mice at intervals after the injection of 30 mmol/kg intraperitoneally; controls received NaCl, 15 mmol/kg. In normal animals brain fructose increased very slowly despite a rapid rise in plasma levels (120 times the control value in 5 min). At 40 min the cerebral level was 1.54 ± 0.23 mmol/kg; the corresponding plasma level was 47.1 ± 4.8 mM. The data suggest that fructose can serve as a source of energy to the brain in times of critical need: during insulin hypoglycemia brain fructose increased to only 0.88 ± 0.05 mmol/kg during the same interval (40 min) despite plasma fructose values equal to those in control animals; also 30 s after cerebral ischemia (decapitation) brain fructose fell from a zero time value of 1.19 ± 0.09 mmol/kg (20 min after fructose injection) to 0.76 ± 0.06 mmol/kg (P= 0.005). Under both circumstances (hypoglycemia and ischemie anoxia) an apparent threshold concentration of fructose for utilization was observed—0.6–0.7 mmol/kg. The most likely explanation for this finding appears to be that this level of fructose was in the extracellular space of the brain. Hexokinase activity in brain homogenates of 8‐ to 12‐day‐old mice with fructose and ATP at concentrations found in vivo and during ischemie anoxia did not appear to be rate‐limiting. We concluded that the major handicap to the use of fructose by the brain was the limited penetration of fructose from the blood to the brain.

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