Decreasing Myocardial Energy Utilization

The onset of myocardial ischemia is followed by the rapid depletion of residual oxygen in the tissues; mitochondrial respiration is inhibited and, within the first 15–30s, the energy metabolism of the cell converts to anaerobic glycolysis [1]. In areas of milder ischemia, some blood glucose may be available as a substrate and the available oxygen may support a reduced level of mitochondrial oxidative metabolism [2]. In areas of severe ischemia, however, the conversion of glycogen to lactate becomes the only meaningful source of high-energy phosphate production. Although the complete oxidation of 1 µmol glucose nets 38µmol ATP, conversion of glycogen to lactate nets only 3µmol ATP per µmol glucosyl units consumed. Thus, anaerobic glycolysis cannot meet the normal energy needs of the working myocardium.