Interventricular redistribution of myocardial blood flow during metabolic vasodilation

To determine the effect of metabolic vasodilation on the blood flow distribution within the hypoperfused left anterior descending coronary artery (LAD) of the pig (a perfusion bed containing both left and right ventricular myocardium), 28 anesthetized (isoflurane) pigs were studied during intracoronary dobutamine infusion (2.5±1, SD, g/min) at two levels of reduced, constant coronary inflow. In 8 pigs, coronary inflow was reduced from 59±9 ml/min to 42±10 ml/ min; coronary perfusion pressure fell to 62±2 mm Hg (8260±260 Pa) and then fell further to 54±6 mm Hg (7190±800 Pa) during dobutamine infusion. Subendocardial blood flow in the anterior wall of the left ventricle perfused by the LAD decreased from 0.64±0.12 ml min^–1g^–1 with hypoperfusion alone, to 0.40±0.14 ml min^–1 g^–1 (P<0.002) with the addition of dobutamine. Conversely, blood flow to the right ventricular region supplied by the LAD increased significantly from 0.78±0.40 ml min^–1 g^–1 (hypoperfusion alone) to 0.92±0.50 ml min^–1 g^–1 (P<0.008) with dobutamine. In 10 pigs, a more severe reduction of coronary inflow to 26±12 ml/min and subsequent dobutamine infusion resulted in a similar redistribution of blood flow from the left to the right ventricular portion of the perfusion bed. Infusion of dobutamine during hypoperfusion, but with a pressure-constant perfusion system, was associated with increases in blood flow to both the right and left ventricular portions of the perfusion territory. Thus, dobutamine could recruit a significant vasodilator reserve throughout the entire perfusion bed including the left ventricular subendocardium. These data demonstrate that the metabolic vasodilation accompanying inotropic stimulation under flow-limited conditions results in an interventricular redistribution, or steal, of blood flow within the LAD perfusion bed.Supported in part by the American Heart Association California Affiliate grant-in-aid 86-S105 and by the National Institutes of Health Research Grant HL-17682, Ischemic Heart Disease Specialized Center of Research (SCOR) awarded by the National Heart, Lung and Blood Institute, Bethesda, MDMr. Schulz was the recipient of a fellowship from Boehringer Ingelheim Fonds. Dr. Guth is currently a Research Fellow with the Alexander von Humboldt-Stiftung, Jean-Paul-Strasse 12, W-5300 Bonn 2, FRGDr. Thaulow was the recipient of a research fellowship granted by The Fogarty International Center Grant 1 FO5 TWo3753-01 BI-5(12)