The relationships among coronary perfusion pressure (0-150 cm H2O), ventricular contracture, vascular resistance, and loss of perfusion of subendocardial myocardium were studied in anoxic isolated rat hearts. Coronary flow and myocardial pH and lactate concentrations were measured during 60 minutes, and the perfusable proportion of the ventricular wall determined after 15 and 60 minutes of global, substrate-free anoxic perfusion. Myocardial contracture in similarly treated hearts was indicated by the pressure exerted on left intraventricular balloons. Decreased perfusion pressure proportionately decreased both coronary flow and the extent of perfusion, and delayed the onset of contracture. The slower development of contracture was associated with a measured increase in lactate content and fall in pH within the ventricular wall. During anoxia the subendocardial myocardium progressively lost its capacity to be perfused, commencing at the onset of ventricular contracture, and continuing to extend even after maximum contracture pressures had been developed. Increased coronary perfusion pressures accelerated the rate of development of contracture but significantly reduced the extent of the perfusion defect, probably by opposing vascular compression.