Reversal of dysfunction in postischemic @entity1562 by XXXX and postextrasystolic potentiation.

@entity1708 @entity7493 @entity308 @entity39 @entity235 @entity1425 @entity63 @entity409 @entity1562 @entity855
After brief coronary occlusions, @entity1562 may become "stunned," exhibiting prolonged @entity308 of function despite the absence of @entity39 . Because of the accompanying decline in @entity855 and @entity1708 precursors, a deficiency of energy supply has been proposed as the basis for @entity409 . This study examined whether sufficient functional and metabolic reserve exists in @entity1562 to sustain a prolonged, maximal inotropic response to @entity1425 and postextrasystolic potentiation. In 11 open chest @entity235 , the left anterior descending coronary artery was occluded for 5 minutes, followed by 10 minutes of reflow, repeated 12 times, with a final 1 hour recovery period. Regional myocardial function was measured using pairs of ultrasonic dimension crystals implanted in @entity63 and nonischemic zones. During repetitive reflows a progressive decrease in mean systolic segment shortening occurred: baseline 21.8%, 1st reflow 15.2%, 12th reflow 4.3%, 1 hour recovery 7.9%. Intravenous @entity1425 , titrated to produce a maximal inotropic response, caused segment shortening to increase to 21.6% after 10 minutes and to 24.8% after 1 hour of infusion, despite a 20 mm Hg increase in systolic pressure. The same dose of @entity1425 given before @entity63 increased segment shortening to 30.5%. In six of the @entity235 , postextrasystolic potentiation before @entity63 increased segment shortening from 21.8 to 31.1%, and after 1 hour of recovery from @entity63 , from 7.9 to 24.8%. Lesser increases in segment shortening were also seen in nonischemic segments. The results indicate that @entity1562 possesses considerable functional reserve. @entity7493 are therefore not likely to be the basis for @entity308 function seen at rest in @entity1562 .
