Virtual electrodes in cardiac tissue: a common mechanism for anodal and cathodal stimulation

J. P. Wikswo*, Shien-Fong Lin, R. A. Abbas

*Corresponding author for this work

Research output: Contribution to journalArticle

284 Scopus citations

Abstract

Traditional cable analyses cannot explain complex patterns of excitation in cardiac tissue with unipolar, extracellular anodal, or cathodal stimuli. Epifluorescence imaging of the transmembrane potential during and after stimulation of both refractory and excitable tissue shows distinctive regions of simultaneous depolarization and hyperpolarization during stimulation that act as virtual cathodes and anodes. The results confirm bidomain model predictions that the onset (make) of a stimulus induces propagation from the virtual cathode, whereas stimulus termination (break) induces it from the virtual anode. In make stimulation, the virtual anode can delay activation of the underlying tissue, whereas in break stimulation this occurs under the virtual cathode. Thus make and break stimulations in cardiac tissue have a common mechanism that is the result of differences in the electrical anisotropy of the intracellular and extracellular spaces and provides clear proof of the validity of the bidomain model.

Original languageEnglish
Pages (from-to)2195-2210
Number of pages16
JournalBiophysical Journal
Volume69
Issue number6
DOIs
StatePublished - 1 Jan 1995

Fingerprint Dive into the research topics of 'Virtual electrodes in cardiac tissue: a common mechanism for anodal and cathodal stimulation'. Together they form a unique fingerprint.

  • Cite this