BACKGROUND: The effects of calcium chloride (CaCl2) on regional mechanical function, coronary blood flow (CBF) and myocardial oxygen consumption (MVO2) were examined in normal and stunned myocardium in an open-chest canine model. The effects were compared with those of epinephrine. METHODS: Thirty-one dogs were acutely instrumented under enflurane anesthesia to measure aortic and left ventricular pressure, pulmonary and left anterior descending (LAD) coronary flow, and subendocardial segment length the in LAD region. CaCl2 (0.1, 0.25, 0.5, 0.75 mg/ml of LAD flow, n = 16) or epinephrine (4, 10, 20, 30 ng/ml of LAD flow, n = 15) was directly infused into the LAD before (normal) and after 15 min of its occlusion and reperfusion (stunned). Simultaneous measurements of arterial and coronary venous contents of oxygen and lactate were made to calculate oxygen (EO2) and lactate (Elac) extraction ratio during CaCl2 or epinephrine infusion. RESULTS: Both CaCl2 and epinephrine infusions in normal myocardium resulted in dose-dependent increases in mechanical functions and MVO2. These changes were accompanied by parallel increases in CBF, resulting in no changes of EO2 with CaCl2, while CBF increased more than MVO2 with epinephrine, resulting in a decrease in EO2. After ischemia and reperfusion, mechanical functions and Elac were significantly depressed, but similar mechanical responses to both agents with resultant unaltered EO2 were observed. Elac was decreased further during epinephrine, while it remained unaltered during CaCl2 infusion in stunned myocardium. CONCLUSIONS: CaCl2, similar to epinephrine, exerts positive inotropic and lusitropic effects in normal and stunned myocardium in dogs. In addition, CaCl2 has no direct effect on coronary vascular tone in either normal or stunned myocardium, while epinephrine causes direct vasodilation in normal but not in stunned myocardium.