The authors studied the effect of halothane in a canine model of coronary collateral circulation secondary to chronic occlusion of a coronary artery. Two sets of experiments were performed. In the first experiments, Ameroid® constrictors were placed around the left anterior descending coronary artery to produce complete occlusion in three weeks. An inflatable occluder was placed around the circumflex coronary artery in order to apply a mild stenosis to the artery supplying the collateral vessels to produce vasodilation distal to the stenosis. Regional myocardial blood flows were measured using radioactive microspheres. Blood flows to normal and collateralized myocardium were decreased significantly during halothane anesthesia, but perfusion of the subendocardium in both regions was maintained even in the presence of mild stenosis of the circumflex coronary artery supplying the collateral vessels, as indicated by unchanged endocardial/epicardial blood flow ratios. In the second experiments, chronic occlusions of both circumflex and right coronary arteries were produced using Ameroid constrictors. In these animals, sedated using xylazine, pacing-induced tachycardia produced a marked but reversible decrease in blood flow to the collateralized subendocardium. During halothane anesthesia at normal heart rate, blood flow to the collateralized subendocardium was well maintained, but tachycardia produced marked decrease in blood flow to the collateralized subendocardium, leading to the demise of four of seven dogs. The authors conclude that in this chronic canine model, in which control measurements were made during sedation using xylazine, coronary collateral blood flow is well maintained during halothane anesthesia at normal heart rate, but tachycardia during halothane anesthesia severely limits blood flow to the collateralized subendocardium.