Changes in contractility fail to alter the size of the functional border zone in anesthetized XXXX .

@entity1169 @entity63 @entity235 @entity1563 @entity3044
The functional border zone is nonischemic myocardium that exhibits reduced function adjacent to an @entity63 area. To determine if the functional border zone can be modified by pharmacologic interventions that alter contractility, we infused @entity3044 (0.04-0.10 micrograms/kg/min) or administered @entity1169 (2 mg/kg) during circumflex @entity1563 in nine anesthetized, open-chest @entity235 . We measured systolic wall thickening on both sides of the perfusion boundary, which was delineated with myocardial blood flow (microsphere) maps constructed from small tissue samples. By fitting sigmoid curves to the composite systolic wall thickening data after @entity1563 , we modeled the distribution of functional impairment across the perfusion boundary. Defined as the distance from the perfusion boundary to 97.5% of the nonischemic asymptote of the sigmoid fits, the functional border zone was 31 degrees of circumference after @entity1563 alone. @entity3044 increased +dP/dt by 58% and augmented nonischemic systolic wall thickening without changing the lateral extent of the functional border zone (32 degrees). @entity1169 reduced +dP/dt by 24% and depressed nonischemic systolic wall thickening, but the size of the functional border zone remained limited to 28 degrees. Within the functional border zone, wall thickening was significantly but only moderately reduced (-28%) compared with thickening in nonischemic myocardium more than 10 mm away from the perfusion boundary. The ratio of nonischemic border zone to central nonischemic area wall thickening remained the same with each intervention. We conclude that the dimensions of the functional border zone are fixed early after @entity1563 and that inotropic interventions do not modify the extent or relative severity of nonischemic regional dysfunction.
