Simulation study of action potentials from metabolically impaired cardiac myocytes

J. M. Ferrero, J. Saiz, J. M. Ferrero, L. M. Roa, Nitish V Thakor

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

The aim of this work is to quantitatively study the role of the ATP-sensitive potassium current (IK-ATP) and its contribution to the electrophysiological changes which occur during metabolic impairment in ventricular cardiac myocytes. For this purpose, we have formulated a model of the IK-ATP current and incorporated it into the Luo-Rudy model of the ventricular cardiac action potential. We simulated action potentials (AP) developed by space-clamped myocytes under different intracellular levels of ATP and ADP. At normal ionic concentrations, only approx.0.6% of the channels, when open, accounted for a 50% reduction in AP duration. Increased levels of intracellular Mg2+ counteract this shortening, while high extracellular potassium has the opposite effect. Our theoretical results show that opening of IK-ATP channels plays a significant role in AP shortening during hypoxic/ischemic episodes, with the fraction of open channels involved being very low (less than 1%).

Original languageEnglish (US)
Title of host publicationComputers in Cardiology
PublisherIEEE
Pages47-50
Number of pages4
StatePublished - 1995
Externally publishedYes
EventProceedings of the 1995 Conference on Computers in Cardiology - Vienna, Austria
Duration: Sep 10 1995Sep 13 1995

Other

OtherProceedings of the 1995 Conference on Computers in Cardiology
CityVienna, Austria
Period9/10/959/13/95

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Adenosinetriphosphate
Cardiac Myocytes
Action Potentials
Adenosine Triphosphate
Potassium
Administrative data processing
Adenosine Diphosphate
Muscle Cells

ASJC Scopus subject areas

  • Software
  • Cardiology and Cardiovascular Medicine

Cite this

Ferrero, J. M., Saiz, J., Ferrero, J. M., Roa, L. M., & Thakor, N. V. (1995). Simulation study of action potentials from metabolically impaired cardiac myocytes. In Computers in Cardiology (pp. 47-50). IEEE.

Simulation study of action potentials from metabolically impaired cardiac myocytes. / Ferrero, J. M.; Saiz, J.; Ferrero, J. M.; Roa, L. M.; Thakor, Nitish V.

Computers in Cardiology. IEEE, 1995. p. 47-50.

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Ferrero, JM, Saiz, J, Ferrero, JM, Roa, LM & Thakor, NV 1995, Simulation study of action potentials from metabolically impaired cardiac myocytes. in Computers in Cardiology. IEEE, pp. 47-50, Proceedings of the 1995 Conference on Computers in Cardiology, Vienna, Austria, 9/10/95.
Ferrero JM, Saiz J, Ferrero JM, Roa LM, Thakor NV. Simulation study of action potentials from metabolically impaired cardiac myocytes. In Computers in Cardiology. IEEE. 1995. p. 47-50
Ferrero, J. M. ; Saiz, J. ; Ferrero, J. M. ; Roa, L. M. ; Thakor, Nitish V. / Simulation study of action potentials from metabolically impaired cardiac myocytes. Computers in Cardiology. IEEE, 1995. pp. 47-50
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AB - The aim of this work is to quantitatively study the role of the ATP-sensitive potassium current (IK-ATP) and its contribution to the electrophysiological changes which occur during metabolic impairment in ventricular cardiac myocytes. For this purpose, we have formulated a model of the IK-ATP current and incorporated it into the Luo-Rudy model of the ventricular cardiac action potential. We simulated action potentials (AP) developed by space-clamped myocytes under different intracellular levels of ATP and ADP. At normal ionic concentrations, only approx.0.6% of the channels, when open, accounted for a 50% reduction in AP duration. Increased levels of intracellular Mg2+ counteract this shortening, while high extracellular potassium has the opposite effect. Our theoretical results show that opening of IK-ATP channels plays a significant role in AP shortening during hypoxic/ischemic episodes, with the fraction of open channels involved being very low (less than 1%).

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