Metabolic control of rat heart glycolysis after acute ischaemia: Fluoracetate treatment and thyroid interactions

Abstract

On the basis of measurements of cardiac glycolytic intermediates from glucose-1-phosphate to pyruvate and the adenosine phosphates, the metabolic regulation of glycolysis in rat heart during 25 s of acute ischaemia was found to be oscillatory, with maximum activity at 20 s. The administration of Na fluoracetate to rats, 10 min before the hearts were subjected to 20 s ischaemia, led to increased glycolytic activity as far as pyruvate kinase and an increase in ATP content with concomitant decreases in ADP and AMP. Under these conditions, hypothyroidism led to a 200% increase in cardiac α-glycerophosphate and an activation of phosphofructokinase, which were not seen 1 week after tri-iodothyronine (T 3) treatment. The activity of hexokinase, measured in vitro, was reduced in hypothyroid rat myocardium but the activities of phosphofructokinase, pyruvate kinase and glucose-6-phosphate, 6-phosphogluconate and α-glycerophosphate dehydrogenases were unchanged. T 3 replacement led to further decreases in hexokinase activity, decreases in phosphofructokinase and α-glycerophosphate-dehydrogenase activities and increases in pyruvate kinase and glucose-6-phosphate and 6-phosphogluconate dehydrogenase activities. These results confirm that thyroid hormones may help to maintain cardiac energy supply during and repair following ischaemia.