ELECTROPHYSIOLOGICAL CHANGES INDUCED BY LYSOPHOSPHATIDYLCHOLINE, AN ISCHEMIC PHOSPHOLIPID CATABOLITE, IN RABBIT ATRIAL AND VENTRICULAR CARDIAC-CELLS

The effects of palmitoyl-lysophosphatidylcholine (LPC) were studied on the cellular electrical activity of rabbit heart preparations. LPC (1 00 mumol/l) caused a considerable enhancement of the automaticity of t he SA nodal and Purkinje fibers and frequently induced irregular firin g in both supraventricular (SA node, atrium, AV junction) and ventricu lar (Purkinje fibers, papillary muscle) myocardial regions. The 'autom atotropic' and arrhythmogenic effects of LPC were accompanied by a len gthening of the atrioventricular conduction time. In ventricular muscl e fibers LPC (100 mumol/1) decreased the resting potential (RP), the m aximum rate of depolarization (V.) and the amplitude (APA) and duratio n (APD) of the action potential, and often evoked action potentials of 'slow response' type. In atrial muscle cells, 100 mumol/l LPC was cap able of inducing hyperpolarization, with concomitant increases in RP, V(max), APA and APD; higher concentrations (300 and 600 mumol/1) of LP C resulted in decreases in RP, V(max), APA and APD, i.e. phenomena sim ilar to those observed with 100 mumol/l LPC in the ventricular myocard ium. The results seem to support the assumption that lysolipids accumu lating in the ischaemic myocardium may play a pathogenetic role in the development of both supraventricular and ventricular dysrhythmias acc ompanying coronary artery occlusion.