title: Effect of gap junction distribution on impulse propagation in a monolayer of myocytes: a model study.
abstract: OBJECTIVE
  To use microstructural computer models to study how four features of myocardial architecture affect propagation: brick wall tissue structures, jutting at cell ends, gap junction distribution and conductance along cell borders, and increased structural discontinuity.
  
  
  RESULTS
  Simulations of longitudinal and transverse plane wave propagation and point propagation were performed in several two-dimensional (2D) microstructural models of adult cardiac tissue. Conduction velocities and maximum upstroke velocities were measured for a range of gap junction conductances and distributions. In tissue models with normal to low connectivity, brick wall architecture and jutting decrease cell-to-cell delay, increase longitudinal conduction velocity, and decrease longitudinal maximum upstroke velocity. Transverse conduction velocity also increases if the overlap or jutting introduces additional lateral (side-to-side) connections between myocytes. Both end-to-end and side-to-side interplicate gap junctions increase longitudinal and transverse conduction velocity; however, side-to-side interplicate gap junctions have the greatest influence on transverse conduction velocity and longitudinal and transverse maximum upstroke velocity.
  
  
  CONCLUSIONS
  The complex structure of myocardium creates additional pathways of current flow that enhance both longitudinal and transverse propagation. These alternative pathways of current help to maintain conduction as connectivity between cells decreases.
authors.affiliation: Department of Biomedical Engineering, Duke University, 136 Hudson Hall, Durham, NC 27708, USA. mlh23@duke.edu
authors.forename: Marjorie Letitia
authors.initials: ML
authors.lastname: Hubbard
authors.forename: Wenjun
authors.initials: W
authors.lastname: Ying
authors.forename: Craig S
authors.initials: CS
authors.lastname: Henriquez
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000328:Adult; D017629:Gap Junctions / Q000473:pathology* / Q000502:physiology; D006329:Heart Conduction System / Q000473:pathology*; D006801:Humans; D007231:Infant, Newborn; D015640:Ion Channel Gating / Q000502:physiology; D008955:Models, Cardiovascular; D032342:Muscle Cells / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*