MODULATION OF PROPAGATION FROM AN ECTOPIC FOCUS BY ELECTRICAL LOAD AND BY EXTRACELLULAR POTASSIUM

We previously developed a technique (R. Kumar, R. Wilders, R. W. Joyne r, H. J. Jongsma, E. E. Verheijck, D. A. Golod, A. C. G. van Ginneken, and W. N. Goolsby. Circulation 94: 833-841, 1996) for study of a math ematical model cell with spontaneous activity, viz. a ''realtime'' sim ulation of a rabbit sinoatrial node cell (SAN model cell; R. Wilders, H. J. Jongsma, and A. C. van Ginneken. Biophys. J. 60: 1202-1216, 1991 ) simultaneously being electrically coupled via our ''coupling clamp'' [H. Sugiura and R. W. Joyner. Am. J. Physiol. 263 (Heart Circ. Physio l. 32): H1591-H1604, 1992] circuit to a real, isolated ventricular myo cyte. We now apply this technique to investigate effects of coupling c onductance (G(c)), cell size, and the modulation of membrane potential by elevated extracellular potassium concentration on the ability of a n ectopic focus, represented by the SAN model cell, to successfully dr ive a ventricular cell. Values of G(c) and the relative sizes of the t wo cells define three possible outcomes: 1) spontaneous pacing of the SAN model cell but not driving of the ventricular cell, 2) cessation o f spontaneous pacing, or 3) pacing of the SAN model cell and driving o f the ventricular cell. Below a critical size of the SAN model cell on ly the first two of these outcomes is possible. Above this critical si ze there is a range of G(c) that allows successful operation of the sy stem as an ectopic focus. Elevation of extracellular potassium concent ration from 4 to 8 mM increases both the lower bound and upper bound o f G(c) for this range. Elevation of extracellular potassium concentrat ion, as commonly observed in myocardial ischemia, may have effects on either inhibiting or releasing from inhibition an ectopic focus.