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The contraction of the myocyte results from the spike in cytoslic free Ca2+ which precedes the contraction spike by some 50 ms. The time-averaged cytosolic free Ca2+ levels remain very low, normally circa 100 nM. EPA reduced the beating rate without altering the amplitude of contractions, as reported. On another myocyte, which had a much slower endogenous beating rate, Fig. 8B shows the effect of LPC (15 µM) on increasing the cytosolic free Ca2+ concentrations and fluctuations and the resulting tachyarrhythmia. The presence of EPA (10 µM) added to the superfusate reduced the cytosolic [Ca2+]i, sufficiently to terminate the tachyarrhythmia, though not to normal concentrations in this experiment. This beneficial effect of EPA to terminate the arrhythmia results from the action of PUFA to inhibit the L-type Ca2+ current (ICa,L), in adult rat cardiomyocytes is shown in Fig. 9. Such excessive cytosolic free Ca2+ fluctuations, as shown in Fig 8B after LPC can induce delayed after-potentials. If the after-potentials become of sufficient magnitude they may activate Na+ channels to initiate aberrant action potentials. If these occur at a vulnerable moment in the electrical cycle of the heart, fatal arrhythmias may occur. Extracellular application of EPA and the other antiarrhythmic polyunsaturated fatty acids, but not saturated or monounsaturated fatty acids produced a prompt and reversible concentration-dependent inhibition of ICa,L.