Suppression of lysophosphatidylcholine-induced abnormal automaticity by verapamil in canine Purkinje fibers.
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 microM) induced concentration-dependent decreases in resting membrane potential, action potential amplitude and maximum upstroke velocity of phase O. The depolarization was not associated with the reduction of the potassium equilibrium potential, which was calculated from the intracellular potassium 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. These results suggest that verapamil may modify the dysrhythmias induced by LPC in ischemic myocardium.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D004285:Dogs; D004558:Electric Stimulation; D006329:Heart Conduction System / Q000187:drug effects*; D008244:Lysophosphatidylcholines / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D011188:Potassium / Q000378:metabolism / Q000502:physiology; D011690:Purkinje Fibers / Q000187:drug effects* / Q000502:physiology; D014700:Verapamil / Q000494:pharmacology*
D008244:Lysophosphatidylcholines; D014700:Verapamil; D011188:Potassium