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

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 7-10^ 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. • Coronary blood flow is uniformly distributed across the left ventricular free wall of the normally perfused heart of the anesthetized dog (1-3), in spite of the observation that blood entering the left coronary circulation during the systolic phase of the cardiac cycle perfuses primarily the epicardial tissue (4). This nonuniform distribution of systolic flow is believed to be due to the transmural gradient of pressure generated by ventricular contraction (4). It would appear, therefore, that to perfuse the ventricular wall uniformly, diastolic coronary blood flow should be preferentially directed to the subendocardial area. Moir and DeBra (5) have postulated that autoregulatory adjustments in vascular tone are responsible for maintaining adequate subendocardial perfusion. If such an autoregulation is the only mechanism involved in adjusting blood flow to regional requirements, dilation of the coronary vasculature would result in From the Cardiopulmonary Institute at Methodist Hospital and the Departments of Physiology and Internal Medicine, University of Texas Health Science Center, Dallas, Texas 75235. This study was supported in part by the Cardiology Fund and the Council for Tobacco Research-U.S.A., Inc., and The American Heart Association Texas Affiliate, Inc. Received January 20, 1975. Accepted for publication April 25, 1975. relative underperfusion of the subendocardium. Earlier investigations (1, 2) have demonstrated that a reduction in vascular tone brought about by restricting coronary blood flow causes subendocardial ischemia. The present investigation was designed to examine the transmural distribution of myocardial blood flow when coronary vascular tone is abolished without restricting coronary blood flow.