Characterization of Shock-Induced Action Potential Extension During Acute Regional Ischemia in Rabbit Hearts

Shock Effects During Ischemia. Introduction: Defibrillation shocks produce extension of the myocardial action potential repolarization time (AP extension) in nonischemic myocardium. AP extension may synchronize repolarization in the heart because the extension increases when shock timing is increased. We tested whether AP extension occurs and whether it increases when shock timing is increased in regionally ischemic isolated perfused rabbit hearts stained with the transmembrane voltage sensitive fluorescent dye, di‐4‐ANEPPS and given diacetyl monoxime to eliminate motion artifacts. Methods and Results: Before and after left anterior descending (LAD) coronary artery occlusion, APs were recorded on the anterior left ventricular epicardium with an epifluorescence measurement system. Hearts were paced with a train of 10 stimuli (SI) and then during the 10th AP were given a defibrillation shock (S2) from epicardial electrodes on either side of the recording region. Before LAD occlusion, duration of the 9th SI‐induced AP measured at full repolarization was 171 ± 11 msec (mean ± SD). Within 15 minutes after LAD occlusion, the AP duration became shorter (P < 0.05) and more variable (137 ± 42 msec), and APs with negligible plateaus were observed. Extension of the 10th AP by S2 was significant both before (mean extension of 59 to 65 msec for three S2 waveforms tested) and after LAD occlusion (mean extension of 35 to 41 msec). Unlike the results before LAD occlusion, AP extension after occlusion was independent of absolute shock timing expressed in msec. When timing was expressed as a fraction of individual AP durations, AP extension after occlusion increased with increases in shock timing. Conclusions: Shocks extend Aps during ischemia; however, absolute time dependence of AP extension is not constant among cells that have different AP durations during Ischemia. This may influence postshock repolarization synchrony when different AP durations exist in different parts of regionally ischemic hearts.