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It has been reported that long chain acyl carnitine accumulates in ischemic myocardium, and L-carnitine prevents ventricular arrhythmias as well as the accumulation of long chain acyl carnitine in ischemic and free fatty acid supplemented hearts. The purpose of this study was to observe the electrophysiological effects of long chain acyl carnitine, and to evaluate the protective effect of L-carnitine on the transmembrane action potential impaired by long chain acyl carnitine. Using standard microelectrode techniques, transmembrane action potentials were recorded from isolated canine papillary muscle. Palmitoyl carnitine (0.3 mM and 0.6 mM) decreased the resting membrane potential, action potential amplitude and maximum upstroke velocity of phase 0, and shortened action potential duration and effective refractory period in a concentration-dependent manner. Application of L-carnitine (25 mM) prevented the effect of palmitoyl carnitine (0.3 mM) on the transmembrane action potential. These results suggest that long chain acyl carnitine plays an important role in arrhythmogenesis, and that the effect is prevented by L-carnitine.

Effects of L-carnitine on action potential of canine papillary muscle impaired by long chain acyl carnitine.