Short periods of coronary artery occlusion are known to produce prolonged periods of ventricular dysfunction. The effects of halothane or isoflurane on contractility and metabolism in postischemic “stunned” myocardium were studied in an open-chest canine model in which the left anterior descending artery (LAD) was occluded for 15 min and then reperfused. Regional function in the LAD and circumflex artery (CIRC) areas were measured with sonomicrometry, and metabolic data were determined from simultaneous arterial and venous measurements of oxygen and lactate. Halothane and isoflurane produced equivalent decreases in systolic shortening in both normal (CIRC) and stunned (LAD) areas of the heart. Furthermore, the amount of depression was similar with either halothane or isoflurane. Halothane 0.75 MAC significantly decreased systolic shortening in both the LAD region (from 38.8 ± 25.9% to 11.0 ± 21.8%) and in the CIRC region (from 116.7 ± 24.7% to 87.5 ± 23.3%). At equivalent MAC concentrations of isoflurane, the values were 42.5 ± 45.7 to −7.0 ± 49.9% in the LAD region and 91.5 ± 11.9% to 66.9 ± 23.9% in the CIRC area. At 1.5-MAC halothane, systolic shortening in the LAD region decreased from 47.9 ± 47.2% to –0.6 ± 20.3% and in the CIRC area from 114.6 ± 16.8% to 76.0 ± 18.7%. Isoflurane at 1.5 MAC produced significant decreases, from 23.4 ± 54.5% to –15.6 ± 27.1% in the LAD region and from 94.4 ± 33.2% to 61.3 ± 28.2% in the CIRC area. High concentrations of isoflurane (1.5 MAC) were associated with decreased lactate extraction (from 40 ± 16% to 32 ± 10%) and decreased oxygen extraction (from 46 ± 8% to 37 ± 11%), whereas halothane administration was not accompanied by any significant change in metabolic parameters. Although the decreases in systolic shortening produced by halothane and isoflurane are similar in normal and stunned myocardium, this depression of function after administration of volatile anesthetic agents may be of greater significance in postischemic stunned myocardium.