REPOSITORIO
INSTITUCIONAL

    • español
    • English
  • Site map
  • English 
    • español
    • English
  • Login
  • Artículos(current)
  • Libros
  • Tesis
  • Trabajos de grado
  • Documentos Institucionales
    • Actas
    • Acuerdos
    • Decretos
    • Resoluciones
  • Multimedia
  • Productos de investigación
  • Acerca de
View Item 
  •   Home
  • Artículos
  • Indexados Scopus
  • View Item
  •   Home
  • Artículos
  • Indexados Scopus
  • View Item
JavaScript is disabled for your browser. Some features of this site may not work without it.

In Silico Study of Gaseous Air Pollutants Effects on Human Atrial Tissue

Thumbnail
Share this
Author
Tobón C.
Pachajoa D.C.
Ugarte J.P.
Saiz J.

Citación

       
TY - GEN T1 - In Silico Study of Gaseous Air Pollutants Effects on Human Atrial Tissue AU - Tobón C. AU - Pachajoa D.C. AU - Ugarte J.P. AU - Saiz J. UR - http://hdl.handle.net/11407/5818 PB - IEEE Computer Society AB - Exposure to gaseous air pollutants such as carbon monoxide (CO), nitric oxide (NO) and sulfur dioxide (SO2) promotes the occurrence of cardiac diseases. Investigations have shown that CO and SO2 block the calcium channel (ICaL) of myocytes. The SO2 also increases the sodium channel (INa), the transient outward (Ito) and inward rectifying (IK1) potassium currents. The NO blocks INa and increases ICaL. We developed concentration dependent equations to simulate the gaseous pollutants effects on the ionic currents. They were incorporated in the Courtemanche model of human atrial cell and in a 2D tissue model. A train of 10 stimuli was applied. The action potential duration (APD) was measured. S1-S2 cross-field protocol was applied to initiate a rotor. The CO and SO2 concentrations from 0 to 1000 uM and NO concentration from 0 to 500 nM were implemented. Six concentration combinations were simulated (cases 1 to 6). The gaseous air pollutants caused an APD shortening and loss of plateau phase of the action potential in a fraction that increases as the pollutant concentration increases. When the highest concentration was applied, the APD decreased by 81%. In the 2D model, from case 4 conditions it was possible to generate rotor, propagating with high stability. These results show pro-arrhythmic effects of gaseous air pollutants. © 2019 Creative Commons. ER - @misc{11407_5818, author = {Tobón C. and Pachajoa D.C. and Ugarte J.P. and Saiz J.}, title = {In Silico Study of Gaseous Air Pollutants Effects on Human Atrial Tissue}, year = {}, abstract = {Exposure to gaseous air pollutants such as carbon monoxide (CO), nitric oxide (NO) and sulfur dioxide (SO2) promotes the occurrence of cardiac diseases. Investigations have shown that CO and SO2 block the calcium channel (ICaL) of myocytes. The SO2 also increases the sodium channel (INa), the transient outward (Ito) and inward rectifying (IK1) potassium currents. The NO blocks INa and increases ICaL. We developed concentration dependent equations to simulate the gaseous pollutants effects on the ionic currents. They were incorporated in the Courtemanche model of human atrial cell and in a 2D tissue model. A train of 10 stimuli was applied. The action potential duration (APD) was measured. S1-S2 cross-field protocol was applied to initiate a rotor. The CO and SO2 concentrations from 0 to 1000 uM and NO concentration from 0 to 500 nM were implemented. Six concentration combinations were simulated (cases 1 to 6). The gaseous air pollutants caused an APD shortening and loss of plateau phase of the action potential in a fraction that increases as the pollutant concentration increases. When the highest concentration was applied, the APD decreased by 81%. In the 2D model, from case 4 conditions it was possible to generate rotor, propagating with high stability. These results show pro-arrhythmic effects of gaseous air pollutants. © 2019 Creative Commons.}, url = {http://hdl.handle.net/11407/5818} }RT Generic T1 In Silico Study of Gaseous Air Pollutants Effects on Human Atrial Tissue A1 Tobón C. A1 Pachajoa D.C. A1 Ugarte J.P. A1 Saiz J. LK http://hdl.handle.net/11407/5818 PB IEEE Computer Society AB Exposure to gaseous air pollutants such as carbon monoxide (CO), nitric oxide (NO) and sulfur dioxide (SO2) promotes the occurrence of cardiac diseases. Investigations have shown that CO and SO2 block the calcium channel (ICaL) of myocytes. The SO2 also increases the sodium channel (INa), the transient outward (Ito) and inward rectifying (IK1) potassium currents. The NO blocks INa and increases ICaL. We developed concentration dependent equations to simulate the gaseous pollutants effects on the ionic currents. They were incorporated in the Courtemanche model of human atrial cell and in a 2D tissue model. A train of 10 stimuli was applied. The action potential duration (APD) was measured. S1-S2 cross-field protocol was applied to initiate a rotor. The CO and SO2 concentrations from 0 to 1000 uM and NO concentration from 0 to 500 nM were implemented. Six concentration combinations were simulated (cases 1 to 6). The gaseous air pollutants caused an APD shortening and loss of plateau phase of the action potential in a fraction that increases as the pollutant concentration increases. When the highest concentration was applied, the APD decreased by 81%. In the 2D model, from case 4 conditions it was possible to generate rotor, propagating with high stability. These results show pro-arrhythmic effects of gaseous air pollutants. © 2019 Creative Commons. OL Spanish (121)
Gestores bibliográficos
Refworks
Zotero
BibTeX
CiteULike
Metadata
Show full item record
Abstract
Exposure to gaseous air pollutants such as carbon monoxide (CO), nitric oxide (NO) and sulfur dioxide (SO2) promotes the occurrence of cardiac diseases. Investigations have shown that CO and SO2 block the calcium channel (ICaL) of myocytes. The SO2 also increases the sodium channel (INa), the transient outward (Ito) and inward rectifying (IK1) potassium currents. The NO blocks INa and increases ICaL. We developed concentration dependent equations to simulate the gaseous pollutants effects on the ionic currents. They were incorporated in the Courtemanche model of human atrial cell and in a 2D tissue model. A train of 10 stimuli was applied. The action potential duration (APD) was measured. S1-S2 cross-field protocol was applied to initiate a rotor. The CO and SO2 concentrations from 0 to 1000 uM and NO concentration from 0 to 500 nM were implemented. Six concentration combinations were simulated (cases 1 to 6). The gaseous air pollutants caused an APD shortening and loss of plateau phase of the action potential in a fraction that increases as the pollutant concentration increases. When the highest concentration was applied, the APD decreased by 81%. In the 2D model, from case 4 conditions it was possible to generate rotor, propagating with high stability. These results show pro-arrhythmic effects of gaseous air pollutants. © 2019 Creative Commons.
URI
http://hdl.handle.net/11407/5818
Collections
  • Indexados Scopus [2005]
All of RI UdeMCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects
My AccountLoginRegister
Statistics GTMView statistics 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