Action potential variation in canine ventricle: A modeling study

Semahat S. Demir; Brian O'Rourke; Gordon F. Tomaselli; Eduardo Marban; Raimond L. Winslow

Action potential variation in canine ventricle: A modeling study

Semahat S. Demir, Brian O'Rourke, Gordon F. Tomaselli, Eduardo Marban, Raimond L. Winslow

Research output: Contribution to journal › Article › peer-review

Abstract

An ionic model of the ventricular cell based on voltage-clamp and action potential data measured experimentally in dog heart has been developed. The model is used to test the hypothesis that spatial variation of the magnitude of I_to1, I_K3, I_to2, and the recovery time constant of I_to1 reported in the literature can account for differences in action potential shape of epicardial (EPI), midmyocardial (M), and endocardial (ENDO) cells. The model results demonstrate that experimentally observed differences in EPI, M, and ENDO cells, that are phase 1 spike, notch, phase 3 repolarizaiion, and rate dependence (0.5-2Hz) of action potential duration (APD), are accounted for by the model. The simulated effects of blocking I_K3 I_Kr and I_to1 also agree with experimental data in M cells. Reduction of I_to1, I_K1 and I_up current magnitudes and increase of I_Naca produce prolongation of the APD in the model similar to that observed during pacing tachycardia-induced heart failure in dogs.

Original language	English (US)
Pages (from-to)	221-224
Number of pages	4
Journal	Computers in Cardiology
Volume	0
Issue number	0
State	Published - 1996
Externally published	Yes

ASJC Scopus subject areas

Computer Science Applications
Cardiology and Cardiovascular Medicine

Cite this

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title = "Action potential variation in canine ventricle: A modeling study",

abstract = "An ionic model of the ventricular cell based on voltage-clamp and action potential data measured experimentally in dog heart has been developed. The model is used to test the hypothesis that spatial variation of the magnitude of Ito1, IK3, Ito2, and the recovery time constant of Ito1 reported in the literature can account for differences in action potential shape of epicardial (EPI), midmyocardial (M), and endocardial (ENDO) cells. The model results demonstrate that experimentally observed differences in EPI, M, and ENDO cells, that are phase 1 spike, notch, phase 3 repolarizaiion, and rate dependence (0.5-2Hz) of action potential duration (APD), are accounted for by the model. The simulated effects of blocking IK3 IKr and Ito1 also agree with experimental data in M cells. Reduction of Ito1, IK1 and Iup current magnitudes and increase of INaca produce prolongation of the APD in the model similar to that observed during pacing tachycardia-induced heart failure in dogs.",

author = "Demir, {Semahat S.} and Brian O'Rourke and Tomaselli, {Gordon F.} and Eduardo Marban and Winslow, {Raimond L.}",

year = "1996",

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T2 - A modeling study

AU - Demir, Semahat S.

AU - O'Rourke, Brian

AU - Tomaselli, Gordon F.

AU - Marban, Eduardo

AU - Winslow, Raimond L.

PY - 1996

Y1 - 1996

N2 - An ionic model of the ventricular cell based on voltage-clamp and action potential data measured experimentally in dog heart has been developed. The model is used to test the hypothesis that spatial variation of the magnitude of Ito1, IK3, Ito2, and the recovery time constant of Ito1 reported in the literature can account for differences in action potential shape of epicardial (EPI), midmyocardial (M), and endocardial (ENDO) cells. The model results demonstrate that experimentally observed differences in EPI, M, and ENDO cells, that are phase 1 spike, notch, phase 3 repolarizaiion, and rate dependence (0.5-2Hz) of action potential duration (APD), are accounted for by the model. The simulated effects of blocking IK3 IKr and Ito1 also agree with experimental data in M cells. Reduction of Ito1, IK1 and Iup current magnitudes and increase of INaca produce prolongation of the APD in the model similar to that observed during pacing tachycardia-induced heart failure in dogs.

AB - An ionic model of the ventricular cell based on voltage-clamp and action potential data measured experimentally in dog heart has been developed. The model is used to test the hypothesis that spatial variation of the magnitude of Ito1, IK3, Ito2, and the recovery time constant of Ito1 reported in the literature can account for differences in action potential shape of epicardial (EPI), midmyocardial (M), and endocardial (ENDO) cells. The model results demonstrate that experimentally observed differences in EPI, M, and ENDO cells, that are phase 1 spike, notch, phase 3 repolarizaiion, and rate dependence (0.5-2Hz) of action potential duration (APD), are accounted for by the model. The simulated effects of blocking IK3 IKr and Ito1 also agree with experimental data in M cells. Reduction of Ito1, IK1 and Iup current magnitudes and increase of INaca produce prolongation of the APD in the model similar to that observed during pacing tachycardia-induced heart failure in dogs.

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Action potential variation in canine ventricle: A modeling study

Abstract

ASJC Scopus subject areas

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