Because isoflurane has been reported to produce coronary steal, we studied 12 open chest, anesthetized (pentobarbital) dogs with critical stenosis (CS) of the left circumflex coronary artery (LCA). Sonomicrometers were implanted to measure systolic wall thickening, myocardial blood flow (MBF) was measured with microspheres (15 μm diameter), and regional venous sampling was performed to estimate regional oxygen extraction and myocardial oxygen consumption (MVO2). Anesthetic concentrations of isoflurane reduced arterial blood pressure dramatically, resulting in a maldistribution of MBF distal to the CS consistent with the pattern characterizing a transmural coronary steal effect. Elevation of arterial blood pressure with phenylephrine during high concentration isoflurane (1.7 ± 0.1%) augmented MBF, but the maldistribution distal to the CS persisted. Despite the maldistribution, however, there was no indication of ischemia in the LCA region because systolic wall thickening, oxygen extraction, and MVO2 were not significantly different between the LCA and left anterior descending coronary artery (LAD) (control) areas. Because wall thickening, oxygen extraction, and MVO2 were markedly reduced by isoflurane in both the LCA and control areas, it was concluded that isoflurane substantially reduced myocardial oxygen requirements by inducing myocardial depression, reducing heart rate, and decreasing afterload. Consequently, the apparent maldistribution of LCA blood flow (coronary steal) was due to the hemodynamic and vasodilatory effects of isoflurane, but did not result in ischemia because the level of blood flow was at or above the requirements of the myocardium.