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In 14 beating hearts, coronary blood flow was measured electromagnetically in either the left circumflex or the left anterior descending coronary artery, and regional myocardial blood flow was computed from tissue uptake of 7−10μ radioactive microspheres. Metabolic dilation of the coronary circulation was induced by occluding the coronary artery for 10 or 90 seconds, and pharmacologic dilation was induced by infusing papaverine into the artery. In seven dogs, differently labeled microspheres were administered (1) before coronary artery occlusion, (2) at the peak reactive hyperemic response to a 10-second coronary artery occlusion, and (3) early in the rising phase of the hyperemic response following a 90-second coronary artery occlusion. Myocardial blood flow was distributed uniformly across the left ventricular free wall before occlusion and at peak hyperemia after the 10-second occlusion, but early in the hyperemic response to the 90-second occlusion coronary blood flow preferentially perfused subepicardial tissue. In another group of seven dogs, microspheres were administered (1) before coronary artery occlusion, (2) at the peak hyperemic flow after a 90-second occlusion, and (3) at the peak flow during local intracoronary infusion of papaverine. The left ventricular free wall was uniformly perfused under each condition. However, in 12 vented, fibrillating hearts with coronary circulations dilated maximally by perfusion with venous blood containing either papaverine or adenosine, left ventricular blood flow was preferentially directed to the subendocardium (endocardial-epicardial ratio averaged 1.37 ± 0.08 [SE]). We conclude that the coronary circulation of the normally functioning canine heart can dilate maximally without causing relative subendocardial ischemia because of a gradient of vascularity that favors the subendocardium and compensates for systolic flow limitation in that region.

Uniformity of transmural perfusion in anesthetized dogs with maximally dilated coronary circulations.