Severe myocardial depression was induced in 12 anesthetized closed-chest dogs by mercury embolization of the left coronary artery and the effects of dopamine infusion (5 μg per kilogram per minute) studied. Coronary embolization produced decreases in cardiac output (CO) of 52 per cent, stroke volume (SV) of 49 per cent, left ventricular peak dP dt ( LVdP dt ) of 29 per cent, stroke work (SW) of 60 per per cent, LV systolic pressure (LVSP) of 14 per cent, and an increase in systemic vascular resistance (SVR) of 77 per cent. LV end-diastolic pressure (LVEDP) increased from 7 to 18 mm. Hg. After 20 minutes of dopamine, CO increased 30 per cent, SV 31 per cent, SW 46 per cent, LVdP dt 64 per cent, and LVSP 8 per cent; SVR decreased 18 per cent and LVEDP was 14 mm. Hg (all changes p < 0.05). Heart rate and mean aortic pressure did not change. After 60 minutes of dopamine, slight deterioration occurred but most parameters were still significantly improved. Thirty minutes after stopping dopamine, marked circulatory deterioration recurred. Persistent ventricular dysrhythmias occurred in 6 dogs, in 4 of whom dopamine dosage had to be decreased to 2.2 μg per kilogram per minute because of persistent ventricular tachycardia. It is concluded that dopamine will improve depressed myocardial function following acute coronary arterial embolization, at least temporarily, but that the incidence of serious ventricular dysrhythmias may well limit its use.