During a 15-minute period of myocardial ischemia, glycogen concentration fell. This decrease was roughly accounted for by increases in hexosemonophosphate and lactic acid. Fructose 1,6-diphosphate, dihydroxyace-tone-phosphate and pyruvate did not accumulate. The myocardial concentration of adenosinetriphosphate declined. Reperfusion of the ischemie heart with oxygenated blood was accompanied by inconstant changes in myocardial glycogen and by rapid lowering of hexosemonophosphate. The hexosemonophosphate decrease occurred even when the ischemie myocardium was perfused with a deoxygenated buffered salt solution and is attributed in part at least to lactic acid washout. Adeno-sinetriphosphate rose steadily when the heart was perfused with oxygenated blood containing 15 mmoles KCl to prevent cardiac activity. When KCl was not added, fibrillation and irregular contractions occurred within 1 to 2 minutes. In these instances, the rise in adenosinetriphosphate was irregular and inconstant.