Postextrasystolic potentiation of regional mechanical performance during prolonged myocardial ischemia in the dog.

The effects of postextrasystolic potentiation (PESP) on the contractile performance of central ischemic and border zones, as well as of nonischemic myocardium, were studied in 14 open-chest dogs sub- jected to a 4-hour left anterior descending coronary artery ligation followed by 1 hour of reperfusion.Intrinsic mechanical function during right ventricular pacing (134 4 3 beats/min) was compared with function in beats after single, closely coupled (179 i 3 msec) extrasystoles throughout ischemia and reperfusion.Regional myocardial blood flow using radioactive microspheres and infarct size using tetrazolium blue staining were also measured in these segments.PESP was capable of augmenting border zone segment performance to control levels throughout 4 hours of ischemia.PESP significantly augmented central ischemic zone segment function throughout ischemia, but not to control levels.After prolonged ischemia, reperfusion improved both regional intrinsic and potentiated mechanical performance in border and ischemic zones.At 4 hours of ischemia, myocardial blood flow decreased 52% (to 60 ml/100 g/min) in the border zone and 78% (to 28 ml/100 g/min) in the ischemic zone.Infarct size (the percentage necrosis of the transmural segment) measured 55 ± 10% and 74 ± 7% in border and ischemic zones, respectively.Thus, in the open-chest dog, PESP elicited considerable contractile reserve in border and ischemic zones during prolonged ischemia, and despite profound ischemic injury, both intrinsic and potentiated mnechanical function in the ischemic zone could be improved after reperfusion.A MAJOR RESEARCH effort using interventions that can reduce the quantity of infarcted tissue after coronary occlusion is under way.1 3 Two physiologic concepts are central to the thesis that ischemic myocardium may be salvageable.1) Permanent damage to myocardial cells does not occur until a finite time after the onset of myocardial ischemia.42) The distribution of the ischemic process in an arca of focal myocardial ischemia is not homogeneous; that is, some cells, particularly the population of cells in