During acute myocardial ischemia, there exists a zone of myocardial dysfunction that surrounds the central ischemic area that has been termed the functional border zone. We hypothesized that this nonischemic but dysfunctional myocardium may respond to an inotropic challenge. To address this issue, we studied 11 open-chest dogs during acute left circumflex (LCx) occlusion. Simultaneous two-dimensional echocardiograms and radioactive microsphere injections were used to create circumferential left ventricular flow-function maps at the papillary muscle level. Serial studies were performed at baseline, 15 min after LCx occlusion, and after the infusion of dobutamine during LCx occlusion. After occlusion, wall thickening decreased from 52 +/- 8% (mean +/- SEM) to -5 +/- 5% (p less than .01) in the central ischemic zone. The extent of left ventricular dysfunction measured 170 +/- 11 degrees while the subendocardial hypoperfusion zone was 130 +/- 9 degrees (p less than .05), resulting in a functional border zone of 40 +/- 11 degrees. During the infusion of dobutamine, wall thickening did not change in the central ischemic zone but increased adjacent to the functional border zone (p less than .01) and in the normal zone (p less than .05), reducing the extent of the functional border zone to 19 +/- 16 degrees (p less than .05). After dobutamine, the slope of transition of wall thickening from nonischemic to ischemic zones, measured directly from the left ventricular function map, increased on the free wall border (0.71 +/- 0.11 to 0.95 +/- 0.10, p less than .02) to a greater extent than on the septal border (0.60 +/- 0.08 to 0.73 +/- 0.06, p = .07). We conclude that nonischemic myocardium adjacent to ischemic tissue responds to inotropic challenge, dobutamine produces a significant decrease in the size of the functional border zone, and dynamic changes in wall thickening after inotropic intervention are greater in the functional border zone of the lateral free wall than at the septal border of the ischemic area.