Twenty-four hours after occlusion of the left anterior descending coro
nary artery in the dog, ventricular tachycardia is the predominant rhy
thm. At this time, records of transmembrane potentials from the subend
ocardial Purkinje fibers adjacent to the infarct show a low maximum di
astolic potential, prominent phase 4 depolarization, and slow response
action potentials. Exposure of the fibers to pinacidil, 25-100 mu M,
increases resting potential to the estimated value of E(K), abolishes
the phase 4 depolarization, and restores action potential amplitude an
d V-max toward normal. Perfusion of the bed of the occluded coronary a
rtery with Tyrode's solution prior to isolation of the subendocardial
tissues results in similar normalization of transmembrane potentials.
These findings indicate: (a) that the major cause of the abnormal tran
smembrane potentials of the subendocardial tissues is the loss of rest
ing potential; and (b) that abnormalities of the transmembrane potenti
als are caused by some substance that can be washed out by perfusion a
nd not by a direct effect of ischemia.