title: Transmembrane potential changes caused by monophasic and biphasic shocks.
abstract: Transmembrane potential change (DeltaVm) during shocks was recorded by a double-barrel microelectrode in 12 isolated guinea pig papillary muscles. After 10 S1 stimuli, square-wave S2 shocks of both polarities were given consisting of 10-ms monophasic and 10/10-ms and 5/5-ms biphasic waveforms that created potential gradients from 1.1 +/- 0.3 to 11.9 +/- 0.4 V/cm. S2 shocks were applied with 30, 60- to 70-, and 90- to 130-ms S1-S2 coupling intervals so that they occurred during the plateau, late portion of the plateau, and phase 3 of the action potential, respectively. Some shocks were given across as well as along the fiber orientation. The shocks caused hyperpolarization with one polarity and depolarization with the opposite polarity. The ratio of the magnitude of hyperpolarization to that of depolarization at the three S1-S2 coupling intervals was 1.5 +/- 0.3, 1.1 +/- 0.2, and 0.5 +/- 0.2, respectively. DeltaVm during the shock was significantly greater for the monophasic than for the two biphasic shocks. The prolongation of total repolarizing time (TRT) was significantly greater for monophasic (119.8 +/- 19.1%) and 10/10-ms biphasic (120.5 +/- 18.2%) than for 5/5-ms biphasic (113.0 +/- 12.9%) waveforms. The dispersion of the normalized TRT between instances of hyperpolarization and depolarization caused by the two shock polarities was 7.4 +/- 7.1% for monophasic, 3.0 +/- 4.1% for 10/10-ms biphasic, and 2.8 +/- 3.1% for 5/5-ms biphasic shocks (P < 0.05 for monophasic vs. biphasic). Shock fields along fibers produced a larger DeltaVm and prolongation of TRT than those across fibers. We conclude that 1) a change in shock polarity causes an asymmetrical change in membrane polarization depending on shock timing; 2) the 5/5-ms biphasic waveform causes the smallest DeltaVm, prolongs repolarization the least, and causes the smallest polarity-dependent dispersion; and 3) the changes in transmembrane potential and repolarization are influenced by fiber orientation.
authors.affiliation: Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
authors.forename: X
authors.initials: X
authors.lastname: Zhou
authors.forename: W M
authors.initials: WM
authors.lastname: Smith
authors.forename: R K
authors.initials: RK
authors.lastname: Justice
authors.forename: J L
authors.initials: JL
authors.lastname: Wayland
authors.forename: R E
authors.initials: RE
authors.lastname: Ideker
mesh_terms: D000818:Animals; D046508:Culture Techniques; D004558:Electric Stimulation; D004594:Electrophysiology; D006168:Guinea Pigs; D006321:Heart / Q000503:physiopathology*; D008564:Membrane Potentials / Q000502:physiology*