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Department of Experimental Cardiology, Masonic Medical Research Laboratory, Utica, New York 13501-1787
Action potentials and whole
cell sodium current were recorded in canine epicardial, midmyocardial,
and endocardial myocytes in normal sodium at 37°C. Tetrodotoxin (TTX)
reduced the action potential duration of midmyocardial cells to a
greater degree than either epicardial or endocardial cells. Whole cell
recordings in potassium-free and very-low-chloride solutions revealed a
slowly decaying current that was completely inhibited by 5 µM TTX or replacement of external and internal sodium with the impermeant cation
N-methyl-D-glucamine. Late sodium current
density at 0 mV was 47% greater in midmyocardial cells and averaged
0.532 ± 0.058 pA/pF in endocardial, 0.463 ± 0.068 pA/pF
in epicardial, and 0.785 ± 0.070 pA/pF in midmyocardial cells.
Neither the frequency dependence of late sodium current nor its
recovery from inactivation exhibited transmural differences. After a
4.5-s pulse to 30 mV, late sodium current recovered with a single
time constant of 140 ms. We conclude that a larger late sodium
conductance in midmyocardial cells will favor longer action potentials
in these cells. More importantly, drugs that slow inactivation of
sodium channels will produce a nonuniform response across the
ventricular wall that is proarrhythmic.
myocytes; transmural heterogeneity; tetrodotoxin-sensitive current; long Q-T syndrome
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