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Collateral blood flow was studied in chronically instrumented awake dogs 11-12 weeks after implantation of ameroid constrictors on the right and left circumflex coronary arteries. Using 7-10 fim radionuclide-labeled microspheres, transmural myocardial blood flow was measured during resting conditions and at similar heart rates during ventricular pacing and treadmill exercise. The absence of significant myocardial fibrosis was verified histologically. Control transmural flow was distributed normally in all dogs. In five dogs a marked maldistribution of flow occurred in the collateral region during pacing and exercise. During pacing, flow to the epicardial layers increased while flow to the endocardial layers was unchanged, resulting in a marked endocardial perfusion deficit. During exercise, flow increased substantially to all transmural layers, but the endocardial perfusion deficit remained. Mean transmural blood flow increased similarly in the collateral and noncoUateral regions during pacing; however, during exercise, mean flow in the collateral region was significantly lower than in the noncollateral region. These data demonstrate that the collateral vessels became flow limiting and functioned inadequately during tachycardia produced by pacing and exercise; i.e., a marked perfusion deficit occurred in the endocardial layer. Blood flow to all layers in the collateral-dependent region was higher during exercise than during pacing, possibly due to exercise-induced vasodilation of the collateral channels. Circ Res 46: 214-220, 1980

Effects of exercise- and pacing-induced tachycardia on coronary collateral flow in the awake dog.