CORONARY AND MYOCARDIAL EFFECTS OF DOPAMINE IN THE CONSCIOUS DOG: PARASYMPATHOLYTIC AUGMENTATION OF PRESSOR AND INOTROPIC ACTIONS

¹ Departments of Medicine, Harvard Medical School and the Peter Bent Brigham Hospital, Department of Cardiology, Children's Hospital Medical Center, Boston, Massachusetts; and the Department of Medicine, University of California, San Diego, California

The effects of intravenous dopamine (3,4-dihydroxyphenylethylamine), 4.0 and 40.0 µg/kg, were studied on coronary blood flow and resistance, left ventricular pressure and diameter, dP/dt, dP/dt/P and on the velocity of myocardial fiber shortening in conscious dogs. Dopamine (40 µg/kg) caused an initial elevation in coronary resistance (41%) associated with increases in mean arterial pressure (26 mm Hg), systolic left ventricular pressure (31 mm Hg), end-diastolic diameter (1.4 mm), dP/dt (3580 to 4620 mm Hg/sec) and dP/dt/P (46 to 52 sec^-1) whereas heart rate fell from 80 to 63 beats/min. The coronary vasoconstrictor response was followed by a late reduction in coronary resistance (-29%) when pressures, dimensions and contractility had returned toward control, but while heart rate was higher than control. With heart rate maintained constant, dopamine (40 µg/kg) caused greater pressor and inotropic effects. Dopamine's pressor and inotropic effects were augmented further following cholinergic blockade, while coronary effects were not affected substantially. The pressor and coronary vasoconstrictor effects were prevented by alpha receptor blockade, while the increases in contractility were prevented by beta receptor blockade. Coronary resistance fell with dopamine after combined alpha and beta receptor blockades, suggesting dopaminergic coronary vasodilatation. In anesthetized, open-chest dogs coronary vasoconstriction was not observed when heart rate was allowed to vary, or was maintained constant, or following cholinergic blockade. Furthermore, the pressor and inotropic effects were similar before and after cholinergic blockade.