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Effects of Elevated Extracellular Potassium on the Stimulation Mechanism of Diastolic Cardiac Tissue

Veniamin Y. Sidorov ^* , Marcella C. Woods  and John P. Wikswo ^*   

^* Department of Physics and Astronomy; Vanderbilt Institute for Integrative Biosystems, Research and Education; Department of Biomedical Engineering; and Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee

Correspondence: Address reprint requests to Dr. John P. Wikswo, Dept. of Physics and Astronomy, Vanderbilt University, VU Station B 351807, Nashville, TN 37235-1807. Tel.: 615-343-4124; Fax: 615-322-4977; E-mail: john.wikswo{at}vanderbilt.edu.

During cardiac disturbances such as ischemia and hyperkalemia, the extracellular potassium ion concentration is elevated. This in turn changes the resting transmembrane potential and affects the excitability of cardiac tissue. To test the hypothesis that extracellular potassium elevation also alters the stimulation mechanism, we used optical fluorescence imaging to examine the mechanism of diastolic anodal unipolar stimulation of cardiac tissue under 4 mM (normal) and 8 mM (elevated) extracellular potassium. We present several visualization methods that are useful for distinguishing between anodal-make and anodal-break excitation. In the 4-mM situation, stimulation occurred by the make, or stimulus-onset, mechanism that involved propagation out of the virtual cathodes. For 8-mM extracellular potassium, the break or stimulus termination mechanism occurred with propagation out of the virtual anode. We conclude that elevated potassium, as might occur in myocardial ischemia, alters not only stimulation threshold but also the excitation mechanism for anodal stimulation.

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