Epinephrine in doses of 0.5 to 1.0 µg/kg/ min has been shown experimentally to augment cardiac output, with increases in both hepatosplanchnic and peripheral blood flow. At these concentrations, the primary effect of epinephrine is cardiotonic, without measurable vasoconstriction. Larger doses produce significant vasoconstriction with a decrease in cardiac output and a reduction in peripheral venous return. The mean rate of excess lactate accumulation was noted to be increased during epinephrine administration in animals with intact circulation, in spite of increased peripheral and hepatosplanchnic blood flow and oxygen consumption. With the heart and lungs functionally excluded by a pump oxygenator, low doses of epinephrine produced no "excess lactate," even though peripheral constriction was measured. Clinical experience indicates that continuous infusion of 0.1 to 0.5 µg/kg/min of epinephrine is effective in the treatment of postoperative low cardiac output syndrome.