REPOSITORIO
INSTITUCIONAL

    • español
    • English
  • Navegar
  • español 
    • español
    • English
  • Acceder
  • Artículos(current)
  • Libros
  • Tesis
  • Trabajos de grado
  • Documentos Institucionales
    • Actas
    • Acuerdos
    • Decretos
    • Resoluciones
  • Multimedia
  • Productos de investigación
  • Acerca de
Ver ítem 
  •   Inicio
  • Artículos
  • Indexados Scopus
  • Ver ítem
  •   Inicio
  • Artículos
  • Indexados Scopus
  • Ver ítem
JavaScript is disabled for your browser. Some features of this site may not work without it.

Sulfur Dioxide Effects on Human Atrial Action Potential: In Silico Study

Thumbnail
Compartir este ítem
Autor
Palacio L.C.
Durango G.
Ugarte J.P.
Saiz J.
Tobon C.

Citación

       
TY - GEN T1 - Sulfur Dioxide Effects on Human Atrial Action Potential: In Silico Study AU - Palacio L.C. AU - Durango G. AU - Ugarte J.P. AU - Saiz J. AU - Tobon C. UR - http://hdl.handle.net/11407/5725 PB - IEEE Computer Society AB - Exposure to air pollutants agents, like sulfur dioxide (SO2), has significant effects on the cardiovascular system. Studies have shown that SO2 blocks ICaL and increases the INa, IK1 and Ito currents, which implies action potential duration (APD) decrease, favoring the initiation of atrial arrhythmias. This study aims to assess the effects of the SO2 at different concentrations on human atrial action potential, using computational simulation. For this, based on experimental data, we developed concentration-dependent equations to simulate the SO2 effects on the currents. They were incorporated in the Courtemanche model of human atrial cell and in a 2D model of atrial tissue. S1-S2 cross-field protocol was applied to initiate a rotor. SO2 concentrations from 0 to 100 ? M were implemented. Our results are in agreement with results from non-human in vitro and in vivo studies. The SO2 causes APD shortening and loss of plateau phase in a fraction that increases as the concentration increases. In the 2D model, a rotor can be generated from 50 ? M of SO2 concentration, showing a pro-arrhythmic effect. © 2018 Creative Commons Attribution. ER - @misc{11407_5725, author = {Palacio L.C. and Durango G. and Ugarte J.P. and Saiz J. and Tobon C.}, title = {Sulfur Dioxide Effects on Human Atrial Action Potential: In Silico Study}, year = {}, abstract = {Exposure to air pollutants agents, like sulfur dioxide (SO2), has significant effects on the cardiovascular system. Studies have shown that SO2 blocks ICaL and increases the INa, IK1 and Ito currents, which implies action potential duration (APD) decrease, favoring the initiation of atrial arrhythmias. This study aims to assess the effects of the SO2 at different concentrations on human atrial action potential, using computational simulation. For this, based on experimental data, we developed concentration-dependent equations to simulate the SO2 effects on the currents. They were incorporated in the Courtemanche model of human atrial cell and in a 2D model of atrial tissue. S1-S2 cross-field protocol was applied to initiate a rotor. SO2 concentrations from 0 to 100 ? M were implemented. Our results are in agreement with results from non-human in vitro and in vivo studies. The SO2 causes APD shortening and loss of plateau phase in a fraction that increases as the concentration increases. In the 2D model, a rotor can be generated from 50 ? M of SO2 concentration, showing a pro-arrhythmic effect. © 2018 Creative Commons Attribution.}, url = {http://hdl.handle.net/11407/5725} }RT Generic T1 Sulfur Dioxide Effects on Human Atrial Action Potential: In Silico Study A1 Palacio L.C. A1 Durango G. A1 Ugarte J.P. A1 Saiz J. A1 Tobon C. LK http://hdl.handle.net/11407/5725 PB IEEE Computer Society AB Exposure to air pollutants agents, like sulfur dioxide (SO2), has significant effects on the cardiovascular system. Studies have shown that SO2 blocks ICaL and increases the INa, IK1 and Ito currents, which implies action potential duration (APD) decrease, favoring the initiation of atrial arrhythmias. This study aims to assess the effects of the SO2 at different concentrations on human atrial action potential, using computational simulation. For this, based on experimental data, we developed concentration-dependent equations to simulate the SO2 effects on the currents. They were incorporated in the Courtemanche model of human atrial cell and in a 2D model of atrial tissue. S1-S2 cross-field protocol was applied to initiate a rotor. SO2 concentrations from 0 to 100 ? M were implemented. Our results are in agreement with results from non-human in vitro and in vivo studies. The SO2 causes APD shortening and loss of plateau phase in a fraction that increases as the concentration increases. In the 2D model, a rotor can be generated from 50 ? M of SO2 concentration, showing a pro-arrhythmic effect. © 2018 Creative Commons Attribution. OL Spanish (121)
Gestores bibliográficos
Refworks
Zotero
BibTeX
CiteULike
Metadatos
Mostrar el registro completo del ítem
Resumen
Exposure to air pollutants agents, like sulfur dioxide (SO2), has significant effects on the cardiovascular system. Studies have shown that SO2 blocks ICaL and increases the INa, IK1 and Ito currents, which implies action potential duration (APD) decrease, favoring the initiation of atrial arrhythmias. This study aims to assess the effects of the SO2 at different concentrations on human atrial action potential, using computational simulation. For this, based on experimental data, we developed concentration-dependent equations to simulate the SO2 effects on the currents. They were incorporated in the Courtemanche model of human atrial cell and in a 2D model of atrial tissue. S1-S2 cross-field protocol was applied to initiate a rotor. SO2 concentrations from 0 to 100 ? M were implemented. Our results are in agreement with results from non-human in vitro and in vivo studies. The SO2 causes APD shortening and loss of plateau phase in a fraction that increases as the concentration increases. In the 2D model, a rotor can be generated from 50 ? M of SO2 concentration, showing a pro-arrhythmic effect. © 2018 Creative Commons Attribution.
URI
http://hdl.handle.net/11407/5725
Colecciones
  • Indexados Scopus [2142]
Todo RI UdeMComunidades & ColeccionesPor fecha de publicaciónAutoresTítulosPalabras claveEsta colecciónPor fecha de publicaciónAutoresTítulosPalabras clave
Mi cuentaAccederRegistro
Estadísticas GTMVer Estadísticas GTM
OFERTA ACADÉMICA
  • Oferta académica completa
  • Facultad de Derecho
  • Facultad de Comunicación
  • Facultad de Ingenierías
  • Facultad de Ciencias Económicas y Administrativas
  • Facultad de Ciencias Sociales y Humanas
  • Facultad de Ciencias Básicas
  • Facultad de Diseño
SERVICIOS
  • Teatro
  • Educación continuada
  • Centro de Idiomas
  • Consultorio Jurídico
  • Centro de Asesorías y Consultorías
  • Prácticas empresariales
  • Operadora Profesional de Certámenes
INVESTIGACIÓN
  • Biblioteca
  • Centros de investigación
  • Revistas científicas
  • Repositorio institucional
  • Universidad - Empresa - Estado - Sociedad

Universidad de Medellín - Teléfono: +57 (4) 590 4500 Ext. 11422 - Dirección: Carrera 87 N° 30 - 65 Medellín - Colombia - Suramérica
© Copyright 2012 ® Todos los Derechos Reservados
Contacto

 infotegra.com