Calcium inhibits the cardiac stimulating properties of dobutamine but not of amrinone

To contrast the effect of increasing blood calcium concentrations on the cardiovascular actions of intravenous β-adrenergic agonist and phosphodiesterase inhibitors, 46 patients recovering from aortocoronary bypass surgery received either dobutamine or amrinone both in the presence and absence of a calcium infusion. Cardiac output, systemic arterial pressure, pulmonary arterial pressure, central venous pressure, pulmonary artery occlusion pressure, heart rate, and blood ionized calcium concentration were measured before and during infusions of dobutamine (2.5 and 5.0 μg/kg/min) and amrinone (0.75 mg/kg bolus + 10 μg/kg/min or 2.25 mg/kg bolus + 20 μg/kg/min). After the initial dobutamine infusion period, patients were randomly and blindly assigned to receive either a calcium or placebo infusion, and the dobutamine infusions were repeated. Because of the long duration of amrinone's actions, the amrinone maintenance infusion was continued while randomized, blinded infusion of either calcium or placebo was added. Dobutamine (5 μg/kg/min) increased cardiac output from 7.1±0.3 L/min to 9.1±0.4 L/min, and increased heart rate from 93±4 beats/min to 107±4 beats/min. Systemic vascular resistance decreased and stroke volume increased. Dobutamine had no significant effects on other hemodynamic values. Amrinone (2.25 mg/kg/bolus + 20 μg/kg/min) increased cardiac output from 5.6±0.4 L/min to 6.9±0.5 L/min, and increased heart rate from 87±3 beats/min to 98±3 beats/min. Amrinone decreased mean arterial pressure, systemic vascular resistance, pulmonary artery occlusion pressure, central venous pressure, and pulmonary artery pressure. Calcium infusion increased arterial pressure (8 to 13 percent) but had no significant effects on any other hemodynamic parameters. Calcium reduced the increase in cardiac output produced by dobutamine by 30 percent, but it did not alter the cardiotonic actions of amrinone. Thus, calcium inhibits the cardiotonic actions of certain β-adrenergic agonists, most likely by interfering with signal transduction through the β-adrenergic receptor complex.