The response of acutely ischemic myocardium to post-extrasystolic potentiation (PESP) was evaluated in 11 mongrel dogs. Mercury-in-silastic length gauges were sutured to the epicardial surface of the left ventricle; left ventricular pressure was determined via an apical large-bore catheter-transducer system and controlled by volume manipulation. The anterior descending coronary artery was then ligated, and single premature atrial contractions were introduced via an external stimulator. Thirty minutes after occlusion, shortening during ejection had decreased an average of 81 +/- 8 per cent, from 1.30 +/- 0.29 to 0.32 +/- 0.05 mm. PESP initially induced a marked restoration toward normal segmental contraction as systolic shortening increased significantly to 1.14 +/- 0.23 mm. Additionally, paradoxic systolic expansion, when present, reverted to a normal pattern of contraction during PESP. Responsiveness to PESP deteriorated progressively with time over 3 hours following occlusion until the muscle became essentially totally unresponsive to this stimulus. It is concluded that a single premature atrial beat may be used to induce PESP and provides an effective stimulus for contractile reserve of acutely dysfunctional ischemic myocardium. Loss of responsiveness to PESP may represent the progression to nonviability following acute ischemia.