Abstract Experiments designed to ascertain the relationship between cardiac rigor and myocardial ATP depletion were performed in excised totally ischemic dog hearts incubated in vitro at 37°C. Spontaneous electrical activity was recorded and left ventricular contractile response and pressure were measured with an intracavitary balloon. As the incubation proceeded, spontaneous electrical and mechanical activity gradually declined and usually ceased after 25 to 30 and 19 to 22 min of total ischemia, respectively. The pressure remained unchanged at 1 to 4 mmHg for about 50 min and then slowly began to increase. A 2 mmHg pressure rise was noted after a mean interval of 63 ± 3 min. About 4 minlater, when the pressure had risen by 5 mmHg, the subendocardial ATP was decreased to 0.62 ± 08 μmol/g weight (11% of control). ATP depletion also occurred, but was less marked in the mid- and subepicardial zones. The left ventricular pressure increased markedly during the next 15 to 20 min, and was associated with continued loss of tissue ATP. When rigor was fully developed after about 90 min of total ischemia, the ventricular myocardium was stiff, the cavitary pressure was about 70 mmHg and the tissue contained virtually no ATP. Increased electrical activity accelerated both ATP loss and the appearance of rigor. Thus, these studies demonstrate that marked depression in myocardial ATP and the apperance of rigor are closely associated phenomena. The onset of irreversible ischemic cell injury has previously been associated with severe ATP depletion. Thus, the onset of cardiac rigor may be a gross marker of both cellular events.