Beneficial effect of amrinone on myocardial oxygen consumption during acute left ventricular failure in dogs

In 11 dogs ischemic left ventricular failure characterized by a 30 percent reduction In cardiac output and a left ventricular end-dlastolic 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 amrlnone 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 Itters/min [mean ± standarddeviation], p <0.05), left ventricular end-dlastolic pressure (from 21.6 ± 3.5 to 11.0 ± 5.4 mm Hg, p <0.05) and peak positive rate of rise of left ventricular pressure [dP/dt](from 1,264 ± 241 to 1,800 ± 458 mm Hg·^?1, p <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·^?1?^?1 after 2 and 20 minutes; respectively, of amrinone compared with 0.124 ± 0.05 during left ventricular failure (both <0.05). The effects of amrinone on left ventricular failure are due to augmented contractility and mild systemic vasodllatation. The reduction in myocardial oxygen consumption during amrlnone-treated left ventricular failure presumably results from a reduction in ventricular wall tension that more than offsets the effect of an Increase in contractility.