Ethanol, infused either intravenously or directly into the coronary arteries of open-chest dogs, produced progressive alterations in left ventricular end-diastolic pressure, enddiastolic volume, end-systolic volume, and ejection fraction. Despite gross visible impairment of left ventricular contractility, there was no change in cardiac output, heart rate, left ventricular systolic pressure, or left ventricular dp/dt. Gradations of myocardial damage were seen with electron microscopy, which indicate that the mitochondria appear to be the most vulnerable organelle. In anaesthetized dogs without thoracotomy, rapid intravenous infusions of ethanol produced progressive elevations of left ventricular end-diastolic pressure and concomitant decreases in ejection fraction which could be maintained by adjustments of the ethanol infusion rate. The use of ethanol as a chemotoxic agent to produce myocardial failure in the dog obviates the difficulties of unpredictability, a high incidence of ventricular fibrillation, and shock as seen in other models.