Effects of hypoxia of 10-45 seconds duration on energy metabolism in the cerebral cortex of unanesthetized and anesthetized rats.

Glycolytic and citric acid cycle intermediates, as well as organic phosphates, were measured in the cerebral cortex of unanesthetized rats following arterial hypoxia (administration of 6-8% O2) of 10 and 20 s duration. There were decreases in glucose-6-phosphate and fructose-6-phosphate, and increases in fructose-1,6-diphosphate, dihydroxyacetone phosphate and 3-phosphoglycerate, even before pyruvate accumulated. Since measurements of the lactate concentration showed that there was an increased glycolytic rate, the results demonstrate that phosphofructokinase was activated. The glycolytic changes were accompanied by, and probably due to, minor changes in phosphocreatine, ATP, ADP and AMP. Experiments of anesthetized animals showed that hypoxia for 45 s was accompanied by signs of phosphofructokinase activation, even if tissue PCO2 was kept constant. It is concluded that, irrespective of the tissue CO2 tension, hypoxia is accompanied by activation of phosphofructokinase which, at least initially, is responsible for the increased glycolytic rate.