The effects of arterial blood pressure and heart rate on myocardial contraction were studied in a canine model of coronary stenosis. Systolic thickening of a region of myocardium supplied by a cannulated coronary artery was used as a measure of oxygen shortage. A glass stenosis in an external perfusion circuit that provided blood to the cannulated vessel was used to limit coronary flow. Mean arterial pressure was controlled by a blood reservoir and phenylephrine infusion and stabilized at four levels: 60, 80, 100, and 120 mmHg. At each blood pressure level, heart rate was increased by ventricular pacing in steps from 50 to 150 beats/min. Systolic thickening was measured at each of the resulting 20 combinations of blood pressure and heart rate. Measurements were made before cannulation, to serve as an unstenosed control, and following cannulation in the presence of moderate and severe stenoses. In the presence of the severe stenosis, ischemic dysfunction occurred when mean arterial pressure was decreased to 60 mmHg. At this pressure, dysfunction was most dramatic at rapid heart rates. In contrast, hypertension to a mean arterial pressure of 120 mmHg was well tolerated in these nonfailing hearts. Importantly, no single value of either blood pressure or heart rate was found to be associated with ischemia. The threshold for rate-induced ischemia depended on the coexisting value of blood pressure andvice versa.Ischemia was absent if mean arterial pressure exceeded heart rate, that is, if the pressure-rateratioexceeded one.