Abstract
Since the introduction of the methods of cell isolation, patch clamping, cell dialysis and intracellular ion indicators, very major advances have been made in understanding the electrophysiology of cardiac cells (for recent reviews see Noble, 1984; Noble & Powell, 1987; Irisawa, Brown & Giles, 1992). As the information has been made sufficiently precise, it has been incorporated into mathematical models, starting with the Purkinje conducting system (DiFrancesco & Noble, 1985), and extending subsequently to sinus node cells (Noble & Noble, 1984; Noble, DiFrancesco & Denyer, 1989), atrial cells (Hilgemann & Noble, 1987; Earm & Noble, 1990) and ventricular cells Noble et al, 1991). These models have proved successful not only in reproducing normal cardiac electrical activity, but also in reconstructing some of the cellular mechanisms of arrhythmia, including ectopic beating in low potassium and cardiac glycosides (Noble, 1991), action potential shortening during ATP depletion (Nichols & Lederer, 1990), and the early after-depolarizations characteristic of potassium blockers and calcium agonists (in preparation).
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Noble, D., Denyer, J., Brown, H., Winslow, R., Kimball, A. (1993). Cardiac Pacemaker Activity: From Single Cells to Modelling the Heart. In: Ostadal, B., Dhalla, N.S. (eds) Heart Function in Health and Disease. Developments in Cardiovascular Medicine, vol 140. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3090-9_8
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DOI: https://doi.org/10.1007/978-1-4615-3090-9_8
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