In 11 dogs ischemic left ventricular failure characterized by a 30 percent reduction in cardiac output and a left ventricular end-diastolic pressure of 18 mm Hg or more was produced by proximal occlusion of the left anterior descending coronary artery followed by serial occlusions of the distal left circumflex coronary artery. Administration of amrinone in an intravenous bolus injection followed by a constant infusion produced improvements in cardiac output (from 1.62 +/- 0.50 to 2.19 +/- 0.52 liters/min [mean +/- standard deviation], p less than 0.05), left ventricular end-diastolic pressure (from 21.6 +/- 3.5 to 11.0 +/- 5.4 mm Hg, p less than 0.05) and peak positive rate of rise of left ventricular pressure [dP/dt] (from 1,264 +/- 241 to 1,800 +/- 458 mm Hg.s-1, p less than 0.05). These improvements were maintained throughout the 20 minute period of therapy. No significant alteration in heart rate or arterial pressure was noted. In parallel with the hemodynamic improvement myocardial oxygen consumption improved to 0.094 +/- 0.05 and 0.092 +/- 0.04 vol.min-1.g-1 after 2 and 20 minutes, respectively, of amrinone compared with 0.124 +/- 0.05 during left ventricular failure (both p less than 0.05). The effects of amrinone on left ventricular failure are due to augmented contractility and mild systemic vasodilatation. The reduction in myocardial oxygen consumption during amrinone-treated left ventricular failure presumably results from a reduction in ventricular wall tension that more than offsets the effect of an increase in contractility.