TY - JOUR
T1 - Computer simulation of the electrotonic modulation of pacemaker activity in the sinoatrial node by atrial muscle
AU - Toyama, Junji
AU - Boyett, Mark R.
AU - Watanabe, Ei Ichi
AU - Honjo, Haruo
AU - Anno, Takafumi
AU - Kodama, Itsuo
PY - 1995
Y1 - 1995
N2 - Electrotonic interaction between the sinoatrial (SA) node and surrounding atrial muscle was investigated in a computer simulation using a modified Oxsoft HEART model (Oxsoft, Oxford, UK). When an SA node cell model was coupled to a passive atrial membrane model (RC circuit) with various coupling conductances (Gc), there was a Gc-dependent prolongation of spontaneous cycle length (SCL). At a sufficiently high value of Gc, the spontaneous activity was finally stopped. A nonlinear relationship between Gc and SCL was obtained, similar to that observed in experiments on rabbit SA node cells. When the muscarinic potassium current (iK,ACh) was activated in the SA node cell model, the coupling-induced inhibition of pacemaker activity was potentiated. Although coupling current and iK,ACh were additive, their effects on SCL were more than additive because of the nonlinear dependence of SCL on net current. A decrease in the input resistance of the atrial membrane model to simulate the activation of iK,ACh in atrial muscle was also shown to potentiate the coupling-induced inhibition of SA node spontaneous activity.
AB - Electrotonic interaction between the sinoatrial (SA) node and surrounding atrial muscle was investigated in a computer simulation using a modified Oxsoft HEART model (Oxsoft, Oxford, UK). When an SA node cell model was coupled to a passive atrial membrane model (RC circuit) with various coupling conductances (Gc), there was a Gc-dependent prolongation of spontaneous cycle length (SCL). At a sufficiently high value of Gc, the spontaneous activity was finally stopped. A nonlinear relationship between Gc and SCL was obtained, similar to that observed in experiments on rabbit SA node cells. When the muscarinic potassium current (iK,ACh) was activated in the SA node cell model, the coupling-induced inhibition of pacemaker activity was potentiated. Although coupling current and iK,ACh were additive, their effects on SCL were more than additive because of the nonlinear dependence of SCL on net current. A decrease in the input resistance of the atrial membrane model to simulate the activation of iK,ACh in atrial muscle was also shown to potentiate the coupling-induced inhibition of SA node spontaneous activity.
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U2 - 10.1016/S0022-0736(95)80060-3
DO - 10.1016/S0022-0736(95)80060-3
M3 - Article
C2 - 8656116
AN - SCOPUS:0029562355
SN - 0022-0736
VL - 28
SP - 212
EP - 215
JO - Journal of Electrocardiology
JF - Journal of Electrocardiology
ER -