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1 Research Center, Montreal Heart Institute, Montreal, Quebec H1T 1C8; 2 Department of Pharmacology, McGill University, Montreal, Quebec H3G 1Y6; 3 Institut de Genie Biomedical, 4 Departement de Medecine, and 5 Departement de Physiologie, Universite de Montréal, Montreal, Quebec H3C 3J7, Canada
Dogs have been
used extensively to study atrial arrhythmias, but there are no
published mathematical models of the canine atrial action potential
(AP). To obtain insights into the ionic mechanisms governing canine
atrial AP properties, we incorporated formulations of K+,
Na+, Ca2+, and Cl
currents, based
on measurements in canine atrial myocytes, into a mathematical model of
the AP. The rate-dependent behavior of model APs corresponded to
experimental measurements and pointed to a central role for L-type
Ca2+ current inactivation in rate adaptation. Incorporating
previously described regional ionic current variations into the model
largely reproduced AP forms characteristic of the corresponding right atrial regions (appendage, pectinate muscle, crista terminalis, and
atrioventricular ring). When ionic alterations induced by tachycardia-dependent remodeling were incorporated, the model reproduced qualitatively the AP features constituting the cellular substrate for atrial fibrillation. We conclude that this ionic model of
the canine atrial AP agrees well with experimental measurements and
gives potential insights into mechanisms underlying functionally important electrophysiological phenomena in canine atrium.
action potential duration; atrial fibrillation; ion channels; rate adaptation; regional heterogeneity; mathematical model
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