Suppression of lysophosphatidylcholine-induced abnormal automaticity by verapamil in canine Purkinje fibers.

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Abstract
Effects of verapamil on electrophysiological alterations induced by lysophosphatidylcholine (LPC), a toxic membrane-derived phospholipid potentially responsible for ischemia-induced arrhythmias, were evaluated in canine Purkinje fibers. LPC (10-160 .mu.M) induced concentration-dependent decreases in resting membrane potential, action potential amplitude and maximum upstroke velocity membrane potential, action potential amplitude and maximum upstroke velocity of phase 0. The depolarization was unassociated with the reduction of the K equilibrium potential, which was calculated from intracellular K ion activities measured by ion-selective electrodes. A graded increase in LPC concentration invariably induced abnormal automaticity arising from depolarized membrane potentials. Although verapamil did not prevent LPC-induced changes in action potential characteristics, it suppressed the appearance of rapid spontaneous activity at reduced membrane potential. Verapamil may modify the dysrhythmias induced by LPC in ischemic myocardium.

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