Why the study?
Do l-carnitine and acetyl-l-carnitine improve electrophysiological derangements induced by palmityl-l-carnitine in isolated canine ventricular muscle compared to disopyramide?
Do l-carnitine and acetyl-l-carnitine improve electrophysiological derangements induced by palmityl-l-carnitine in isolated canine ventricular muscle compared to disopyramide?
L-carnitine and acetyl-l-carnitine, unlike disopyramide, can ameliorate palmityl-l-carnitine-induced electrophysiological derangements in canine ventricular muscle.
May ameliorate ischemia-related electrophysiological instability in ventricular muscle; leaves open translation to human arrhythmia therapy.
Using the microelectrode technique, the effects of l-carnitine (LC) and acetyl-l-carnitine (ALC) on the changes in the transmembrane action potential of the canine ventricular muscle induced by palmityl-l-carnitine (PLC) were studied in comparison with those of disopyramide (D). LC (5 X 10(-3) M) itself had no effect on the electrophysiological parameters of the ventricular muscle. ALC (5 X 10(-3) M) increased the maximum rate of rise (dV/dt max) slightly and decreased the action potential duration (APD), although these changes were not statistically significant. D (1.5 X 10(-3) M) decreased dV/dt max and prolonged APD and the absolute refractory period (ARP). PLC (3 X 10(-4) M) decreased the resting membrane potential, action potential amplitude and dV/dt max, and it shortened APD and ARP. LC and ALC (5 X 10(-3) M) improved the electrophysiological derangement produced by PLC to the same degree. On the other hand, application of D (1.5 X 10(-5) M) resulted in no improvement of the electrophysiological derangement produced by PLC.
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Matsui et al. (1985) studied this question.
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