Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study

Lead (Pb++) is a toxic agent that can exert adverse effects on the cardiac human health. Pb++ blocks the Ltype Ca++ channels. A decrease in L-type calcium current (ICaL) is an important mechanism favoring atrial fibrillation. It is important to study the electrophysiological Pb++ effects on the atri...

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Fecha de publicación:
2017
Institución:
Universidad de Medellín
Repositorio:
Repositorio UDEM
Idioma:
eng
OAI Identifier:
oai:repository.udem.edu.co:11407/4263
Acceso en línea:
http://hdl.handle.net/11407/4263
Palabra clave:
Atrial fibrillation
In silico models
L-type Ca++ current
Lead (Pb++)
Biomedical engineering
Calcium
Diseases
Electrophysiology
Action potential durations
Action potentials
Adverse effect
Atrial fibrillation
Calcium current
Healthy people
In-silico models
Toxic agents
Lead
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http://purl.org/coar/access_right/c_16ec
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oai_identifier_str oai:repository.udem.edu.co:11407/4263
network_acronym_str REPOUDEM2
network_name_str Repositorio UDEM
repository_id_str
dc.title.spa.fl_str_mv Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study
title Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study
spellingShingle Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study
Atrial fibrillation
In silico models
L-type Ca++ current
Lead (Pb++)
Biomedical engineering
Calcium
Diseases
Electrophysiology
Action potential durations
Action potentials
Adverse effect
Atrial fibrillation
Calcium current
Healthy people
In-silico models
Toxic agents
Lead
title_short Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study
title_full Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study
title_fullStr Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study
title_full_unstemmed Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study
title_sort Lead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico study
dc.contributor.affiliation.spa.fl_str_mv Tobón, C., MATBIOM, Universidad de Medellín, Medellín, Colombia
Pachajoa, D., GI2B, Instituto Tecnológico Metropolitano, Medellín, Colombia
Ugarte, J.P., Grupo de Dinámica Cardiovascular, Universidad Pontificia Bolivariana, Medellín, Colombia
Saiz, J., CI2B, Universitat Politècnica de València, Valencia, Spain
dc.subject.keyword.eng.fl_str_mv Atrial fibrillation
In silico models
L-type Ca++ current
Lead (Pb++)
Biomedical engineering
Calcium
Diseases
Electrophysiology
Action potential durations
Action potentials
Adverse effect
Atrial fibrillation
Calcium current
Healthy people
In-silico models
Toxic agents
Lead
topic Atrial fibrillation
In silico models
L-type Ca++ current
Lead (Pb++)
Biomedical engineering
Calcium
Diseases
Electrophysiology
Action potential durations
Action potentials
Adverse effect
Atrial fibrillation
Calcium current
Healthy people
In-silico models
Toxic agents
Lead
description Lead (Pb++) is a toxic agent that can exert adverse effects on the cardiac human health. Pb++ blocks the Ltype Ca++ channels. A decrease in L-type calcium current (ICaL) is an important mechanism favoring atrial fibrillation. It is important to study the electrophysiological Pb++ effects on the atrial action potential in healthy people and those with AF. For this, we study the consequences of Pb++ on action potential, under normal and atrial fibrillation condition using in silico models. Our results suggest that Pb++ blocks ICaL current in a fraction greater as the concentration increases, resulting in an action potential duration shortening, Pb++ has a greater action potential duration effect on control conditions. To our knowledge, this is the first work that has developed mathematical models of Pb++ effect on ICaLcurrent to study its effect on human atrial action potential. © Springer Nature Singapore Pte Ltd. 2017.
publishDate 2017
dc.date.accessioned.none.fl_str_mv 2017-12-19T19:36:42Z
dc.date.available.none.fl_str_mv 2017-12-19T19:36:42Z
dc.date.created.none.fl_str_mv 2017
dc.type.eng.fl_str_mv Conference Paper
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dc.identifier.isbn.none.fl_str_mv 9789811040856
dc.identifier.issn.none.fl_str_mv 16800737
dc.identifier.uri.none.fl_str_mv http://hdl.handle.net/11407/4263
dc.identifier.doi.none.fl_str_mv 10.1007/978-981-10-4086-3_17
dc.identifier.reponame.spa.fl_str_mv reponame:Repositorio Institucional Universidad de Medellín
dc.identifier.instname.spa.fl_str_mv instname:Universidad de Medellín
identifier_str_mv 9789811040856
16800737
10.1007/978-981-10-4086-3_17
reponame:Repositorio Institucional Universidad de Medellín
instname:Universidad de Medellín
url http://hdl.handle.net/11407/4263
dc.language.iso.none.fl_str_mv eng
language eng
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dc.relation.ispartofes.spa.fl_str_mv IFMBE Proceedings
IFMBE Proceedings Volume 60, 2017, Pages 66-69
dc.relation.references.spa.fl_str_mv Revealing the costs of air pollution from industrial facilities in europe. (2011). Revealing the Costs of Air Pollution from Industrial Facilities in Europe.
Acosta, G. B., & Rubio, M. C. (1990). Effects of lead nitrate on isolated rat atria. [Efecto del nitrato de plomo en aurículas aisladas de rata] Acta Physiologica Et Pharmacologica Latinoamericana, 40(2), 137-148.
Ansari, M. A., Maayah, Z. H., Bakheet, S. A., El-Kadi, A. O., & Korashy, H. M. (2013). The role of aryl hydrocarbon receptor signaling pathway in cardiotoxicity of acute lead intoxication in vivo and in vitro rat model. Toxicology, 306, 40-49. doi:10.1016/j.tox.2013.01.024
Barbosa Jr., F., Sertorio, J. T. C., Gerlach, R. F., & Tanus-Santos, J. E. (2006). Clinical evidence for lead-induced inhibition of nitric oxide formation. Archives of Toxicology, 80(12), 811-816. doi:10.1007/s00204-006-0111-3
Bernal, J., Lee, J. -., Cribbs, L. L., & Perez-Reyes, E. (1997). Full reversal of pb++ block of L-type ca++ channels requires treatment with heavy metal antidotes. Journal of Pharmacology and Experimental Therapeutics, 282(1), 172-180.
Bhatnagar, A. (2004). Cardiovascular pathophysiology of environmental pollutants. American Journal of Physiology - Heart and Circulatory Physiology, 286(2 55-2), H479-H485.
Courtemanche, M., Ramirez, R. J., & Nattel, S. (1998). Ionic mechanisms underlying human atrial action potential properties: Insights from a mathematical model. American Journal of Physiology - Heart and Circulatory Physiology, 275(1 44-1), H301-H321.
Courtemanche, M., Ramirez, R. J., & Nattel, S. (1999). Ionic targets for drug therapy and atrial fibrillation-induced electrical remodeling: Insights from a mathematical model. Cardiovascular Research, 42(2), 477-489. doi:10.1016/S0008-6363(99)00034-6
Dinanian, S., Boixel, C., Juin, C., Hulot, J. -., Coulombe, A., Rücker-Martin, C., . . . Hatem, S. N. (2008). Downregulation of the calcium current in human right atrial myocytes from patients in sinus rhythm but with a high risk of atrial fibrillation. European Heart Journal, 29(9), 1190-1197. doi:10.1093/eurheartj/ehn140
Goralnick, E., & Bontempo, L. J. (2015). Atrial fibrillation. Emergency Medicine Clinics of North America, 33(3), 597-612. doi:10.1016/j.emc.2015.04.008
Kopp, S. J., Baker, J. C., D'Agrosa, L. S., & Hawley, P. L. (1978). Simultaneous recording of his bundle electrogram, electrocardiogram, and systolic tension from intact modified langendorff rat heart preparations I: Effects of perfusion time, cadmium, and lead. Toxicology and Applied Pharmacology, 46(2), 475-487. doi:10.1016/0041-008X(78)90093-5
Patrick, L. (2006). Lead toxicity part II: The role of free radical damage and the use of antioxidants in the pathology and treatment of lead toxicity. Alternative Medicine Review, 11(2), 114-127.
Prentice, R. C., & Kopp, S. J. (1985). Cardiotoxicity of lead at various perfusate calcium concentrations: Functional and metabolic responses of the perfused rat heart. Toxicology and Applied Pharmacology, 81(3 PART 1), 491-501. doi:10.1016/0041-008X(85)90420-X
Rodrigue, J. P. (2013). Pollutants emitted by transport systems (air, water and noise). Pollutants Emitted by Transport Systems (Air, Water and Noise).
Tsao, D. -., Yu, H. -., Cheng, J. -., Ho, C. -., & Chang, H. -. (2000). The change of β-adrenergic system in lead-induced hypertension. Toxicology and Applied Pharmacology, 164(2), 127-133. doi:10.1006/taap.1999.8871
Van Wagoner, D. R. (2003). Electrophysiological remodeling in human atrial fibrillation. PACE - Pacing and Clinical Electrophysiology, 26(7 II), 1572-1575.
Van Wagoner, D. R., Pond, A. L., Lamorgese, M., Rossie, S. S., McCarthy, P. M., & Nerbonne, J. M. (1999). Atrial L-type Ca2+ currents and human atrial fibrillation. Circulation Research, 85(5), 428-436.
Vaziri, N. D., Liang, K., & Ding, Y. (1999). Increased nitric oxide inactivation by reactive oxygen species in lead- induced hypertension. Kidney International, 56(4), 1492-1498. doi:10.1046/j.1523-1755.1999.00670.x
dc.rights.coar.fl_str_mv http://purl.org/coar/access_right/c_16ec
rights_invalid_str_mv http://purl.org/coar/access_right/c_16ec
dc.publisher.spa.fl_str_mv Springer Verlag
dc.publisher.faculty.spa.fl_str_mv Facultad de Ciencias Básicas
dc.source.spa.fl_str_mv Scopus
institution Universidad de Medellín
repository.name.fl_str_mv Repositorio Institucional Universidad de Medellin
repository.mail.fl_str_mv repositorio@udem.edu.co
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spelling 2017-12-19T19:36:42Z2017-12-19T19:36:42Z2017978981104085616800737http://hdl.handle.net/11407/426310.1007/978-981-10-4086-3_17reponame:Repositorio Institucional Universidad de Medellíninstname:Universidad de MedellínLead (Pb++) is a toxic agent that can exert adverse effects on the cardiac human health. Pb++ blocks the Ltype Ca++ channels. A decrease in L-type calcium current (ICaL) is an important mechanism favoring atrial fibrillation. It is important to study the electrophysiological Pb++ effects on the atrial action potential in healthy people and those with AF. For this, we study the consequences of Pb++ on action potential, under normal and atrial fibrillation condition using in silico models. Our results suggest that Pb++ blocks ICaL current in a fraction greater as the concentration increases, resulting in an action potential duration shortening, Pb++ has a greater action potential duration effect on control conditions. To our knowledge, this is the first work that has developed mathematical models of Pb++ effect on ICaLcurrent to study its effect on human atrial action potential. © Springer Nature Singapore Pte Ltd. 2017.engSpringer VerlagFacultad de Ciencias Básicashttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85018384836&doi=10.1007%2f978-981-10-4086-3_17&partnerID=40&md5=5ad5b61b412e38f00f9528d881e9d054IFMBE ProceedingsIFMBE Proceedings Volume 60, 2017, Pages 66-69Revealing the costs of air pollution from industrial facilities in europe. (2011). Revealing the Costs of Air Pollution from Industrial Facilities in Europe.Acosta, G. B., & Rubio, M. C. (1990). Effects of lead nitrate on isolated rat atria. [Efecto del nitrato de plomo en aurículas aisladas de rata] Acta Physiologica Et Pharmacologica Latinoamericana, 40(2), 137-148.Ansari, M. A., Maayah, Z. H., Bakheet, S. A., El-Kadi, A. O., & Korashy, H. M. (2013). The role of aryl hydrocarbon receptor signaling pathway in cardiotoxicity of acute lead intoxication in vivo and in vitro rat model. Toxicology, 306, 40-49. doi:10.1016/j.tox.2013.01.024Barbosa Jr., F., Sertorio, J. T. C., Gerlach, R. F., & Tanus-Santos, J. E. (2006). Clinical evidence for lead-induced inhibition of nitric oxide formation. Archives of Toxicology, 80(12), 811-816. doi:10.1007/s00204-006-0111-3Bernal, J., Lee, J. -., Cribbs, L. L., & Perez-Reyes, E. (1997). Full reversal of pb++ block of L-type ca++ channels requires treatment with heavy metal antidotes. Journal of Pharmacology and Experimental Therapeutics, 282(1), 172-180.Bhatnagar, A. (2004). Cardiovascular pathophysiology of environmental pollutants. American Journal of Physiology - Heart and Circulatory Physiology, 286(2 55-2), H479-H485.Courtemanche, M., Ramirez, R. J., & Nattel, S. (1998). Ionic mechanisms underlying human atrial action potential properties: Insights from a mathematical model. American Journal of Physiology - Heart and Circulatory Physiology, 275(1 44-1), H301-H321.Courtemanche, M., Ramirez, R. J., & Nattel, S. (1999). Ionic targets for drug therapy and atrial fibrillation-induced electrical remodeling: Insights from a mathematical model. Cardiovascular Research, 42(2), 477-489. doi:10.1016/S0008-6363(99)00034-6Dinanian, S., Boixel, C., Juin, C., Hulot, J. -., Coulombe, A., Rücker-Martin, C., . . . Hatem, S. N. (2008). Downregulation of the calcium current in human right atrial myocytes from patients in sinus rhythm but with a high risk of atrial fibrillation. European Heart Journal, 29(9), 1190-1197. doi:10.1093/eurheartj/ehn140Goralnick, E., & Bontempo, L. J. (2015). Atrial fibrillation. Emergency Medicine Clinics of North America, 33(3), 597-612. doi:10.1016/j.emc.2015.04.008Kopp, S. J., Baker, J. C., D'Agrosa, L. S., & Hawley, P. L. (1978). Simultaneous recording of his bundle electrogram, electrocardiogram, and systolic tension from intact modified langendorff rat heart preparations I: Effects of perfusion time, cadmium, and lead. Toxicology and Applied Pharmacology, 46(2), 475-487. doi:10.1016/0041-008X(78)90093-5Patrick, L. (2006). Lead toxicity part II: The role of free radical damage and the use of antioxidants in the pathology and treatment of lead toxicity. Alternative Medicine Review, 11(2), 114-127.Prentice, R. C., & Kopp, S. J. (1985). Cardiotoxicity of lead at various perfusate calcium concentrations: Functional and metabolic responses of the perfused rat heart. Toxicology and Applied Pharmacology, 81(3 PART 1), 491-501. doi:10.1016/0041-008X(85)90420-XRodrigue, J. P. (2013). Pollutants emitted by transport systems (air, water and noise). Pollutants Emitted by Transport Systems (Air, Water and Noise).Tsao, D. -., Yu, H. -., Cheng, J. -., Ho, C. -., & Chang, H. -. (2000). The change of β-adrenergic system in lead-induced hypertension. Toxicology and Applied Pharmacology, 164(2), 127-133. doi:10.1006/taap.1999.8871Van Wagoner, D. R. (2003). Electrophysiological remodeling in human atrial fibrillation. PACE - Pacing and Clinical Electrophysiology, 26(7 II), 1572-1575.Van Wagoner, D. R., Pond, A. L., Lamorgese, M., Rossie, S. S., McCarthy, P. M., & Nerbonne, J. M. (1999). Atrial L-type Ca2+ currents and human atrial fibrillation. Circulation Research, 85(5), 428-436.Vaziri, N. D., Liang, K., & Ding, Y. (1999). Increased nitric oxide inactivation by reactive oxygen species in lead- induced hypertension. Kidney International, 56(4), 1492-1498. doi:10.1046/j.1523-1755.1999.00670.xScopusLead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico studyConference Paperinfo:eu-repo/semantics/conferenceObjecthttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_c94fTobón, C., MATBIOM, Universidad de Medellín, Medellín, ColombiaPachajoa, D., GI2B, Instituto Tecnológico Metropolitano, Medellín, ColombiaUgarte, J.P., Grupo de Dinámica Cardiovascular, Universidad Pontificia Bolivariana, Medellín, ColombiaSaiz, J., CI2B, Universitat Politècnica de València, Valencia, SpainTobón C.Pachajoa D.Ugarte J.P.Saiz J.MATBIOM, Universidad de Medellín, Medellín, ColombiaGI2B, Instituto Tecnológico Metropolitano, Medellín, ColombiaGrupo de Dinámica Cardiovascular, Universidad Pontificia Bolivariana, Medellín, ColombiaCI2B, Universitat Politècnica de València, Valencia, SpainAtrial fibrillationIn silico modelsL-type Ca++ currentLead (Pb++)Biomedical engineeringCalciumDiseasesElectrophysiologyAction potential durationsAction potentialsAdverse effectAtrial fibrillationCalcium currentHealthy peopleIn-silico modelsToxic agentsLeadLead (Pb++) is a toxic agent that can exert adverse effects on the cardiac human health. Pb++ blocks the Ltype Ca++ channels. A decrease in L-type calcium current (ICaL) is an important mechanism favoring atrial fibrillation. It is important to study the electrophysiological Pb++ effects on the atrial action potential in healthy people and those with AF. For this, we study the consequences of Pb++ on action potential, under normal and atrial fibrillation condition using in silico models. Our results suggest that Pb++ blocks ICaL current in a fraction greater as the concentration increases, resulting in an action potential duration shortening, Pb++ has a greater action potential duration effect on control conditions. To our knowledge, this is the first work that has developed mathematical models of Pb++ effect on ICaLcurrent to study its effect on human atrial action potential. © Springer Nature Singapore Pte Ltd. 2017.http://purl.org/coar/access_right/c_16ec11407/4263oai:repository.udem.edu.co:11407/42632020-05-27 17:50:21.113Repositorio Institucional Universidad de Medellinrepositorio@udem.edu.co

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