Abstract
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$^+$, Ca$^2+$, 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 Ca$^2+$
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.
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