Line stimulation parallel to myofibers enhances regional uniformity of transmembrane voltage changes in rabbit hearts.
The sign of transmembrane voltage (Vm) change (delta Vm) in the heart during unipolar point stimulation is nonuniform, which introduces dispersion of states of Vm-dependent ion channels that depends on fiber orientation. We hypothesized that line stimulation parallel to cardiac fibers increases regional uniformity of the delta Vm sign. To test this, we evaluated electrode current distribution and delta Vm produced by unipolar line stimulation in isolated rabbit hearts. The Vm-sensitive fluorescent dye, di-4-ANEPPS, and a laser scanner provided delta Vm measurements at 63 spots in an 8 x 8-mm epicardial region. Line stimulation was tested at specific angles with respect to the fiber direction. Current peaks occurred at electrode ends. For electrodes parallel to fibers (0 degree), epicardium in regions beyond the ends exhibited a nonuniform delta Vm sign, whereas epicardium between the ends exhibited a uniform delta Vm sign that was essentially negative (hyperpolarized) during anodal pulses and positive (depolarized) during cathodal pulses. The delta Vm sign between the ends became less uniform when the stimulation angle was increased relative to the long axis of the fibers. At 90 degrees, the delta Vm sign between the ends was nonuniform and was frequently opposite, near versus away from the electrode. Spatial distributions of delta Vm during line stimulation were qualitatively predictable from anisotropic effects of point stimulation provided that combined effects of points along the electrode and points with higher current near ends were considered. For biphasic line stimulation, delta Vm during the second phase was weakly correlated with the temporal sum of effects of phases given individually, indicating limited ability of summation to predict delta Vm. Thus, uniformity of the delta Vm sign during stimulation is enhanced in the region between the ends of a line electrode parallel to fibers. This may lessen arrhythmogenic dispersion of Vm-dependent ion channel states in the region.
Knisley
S B
SB
Department of Biomedical Engineering, School of Medicine, University of Alabama, Birmingham 35294-0019, USA. sbk@crml.uab.edu
Baynham
T C
TC
D000200:Action Potentials; D000818:Animals; D003198:Computer Simulation; D004558:Electric Stimulation; D005456:Fluorescent Dyes; D006321:Heart / Q000502:physiology*; D008954:Models, Biological; D018485:Muscle Fibers, Skeletal / Q000502:physiology*; D011726:Pyridinium Compounds; D011817:Rabbits
D005456:Fluorescent Dyes; D011726:Pyridinium Compounds; C050019:1-(3-sulfonatopropyl)-4-(beta)(2-(di-n-butylamino)-6-naphthylvinyl)pyridinium betaine