Severe myocardial injury was produced in eight anesthetized dogs by the injection of microspheres into the coronary circulation. Cardiac output and renal blood flow were monitored continuously with electromagnetic flow probes around the ascending thoracic aorta and left renal artery respectively. Intravenous infusions of isoproterenol and of dopamine (0.01–0.64 and 0.4–32.0 μg/kg per minute respectively) produced an increase in the cardiac output. Renal blood flow increased with small doses of isoproterenol but tended to decrease with higher doses; in contrast, all doses of dopamine increased renal blood flow. Dopamine was more effective in raising the systemic arterial blood pressure, but also increased cardiac work. Occasional extrasystoles were induced at higher doses of both amines. In three unanesthetized dogs sensitized by prior ligation of a coronary artery, the largest doses of dopamine tested (24–64 μg/kg per minute) did not produce cardiac arrhythmias. However, when dopamine was given to anesthetized dogs during vagal-induced cardiac slowing (a condition conducive to the emergence of ventricular automaticity), arrhythmias were induced. These data suggest that dopamine can increase both cardiac output and renal blood flow after severe myocardial injury, and may be a rational agent in the treatment of cardiogenic shock. Its arrhythmogenic properties would not appear to restrict its use.