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Glycolysis and the Permeation of Glucose and Lactate in the Isolated, Perfused Dog Brain during Anoxia and Postanoxic Recovery

From the ¹ From the Departments of Physiology and Neurosurgery, University of Wisconsin, Madison, Wisconsin, 53706

Isolated, perfused canine brain preparations were used to investigate cerebral metabolism during anoxia and subsequent recovery. The metabolic response of a 6-min perfusion with anoxic blood (p_oo2 < 10 mm Hg), followed by perfusion for up to 2 hours with normal oxygenated blood, was investigated in 41 separate experiments. Net uptake of glucose and efflux of lactate were calculated from their arteriovenous differences. Concentrations of the glycolytic intermediates, the adenine nucleotides, and glycogen were determined from analyses of cerebral cortex samples which were frozen in situ.

In the canine brain there is approximately a 5-fold increase in the glycolytic rate after 1 min of anoxia. During this period, the rate of glucose uptake increases 140% by a mechanism which appears to be metabolically controlled. The regulatory enzymes hexokinase, phosphofructokinase, and glycogen phosphorylase are also markedly stimulated. Although brain lactic acid increases from 1.78 to 16.1 µmoles per g during anoxia, the increase in lactate efflux from the brain is minimal. Six minutes of anoxia causes the adenylate energy charge to decrease from 0.89 to 0.56.

As a result of aerobic perfusion following anoxia, the adenylate energy charge and the rate of glucose uptake return to normal within about 5 min. The rates of hexokinase and phosphofructokinase are clearly and significantly impeded, which serves to decrease the glycolytic flux. During the 2-hour recovery period, the rate of glycolysis and the levels of glycolytic intermediates return to normal, except for lactate, pyruvate, and glucose 6-phosphate which remain elevated. No net synthesis of glycogen occurs. An inhibiting effect of halothane anesthesia on brain phosphofructokinase was also observed.

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