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

dc.creatorTobón C.spa
dc.creatorPachajoa D.spa
dc.creatorUgarte J.P.spa
dc.creatorSaiz J.spa
dc.date.accessioned2017-12-19T19:36:42Z
dc.date.available2017-12-19T19:36:42Z
dc.date.created2017
dc.identifier.isbn9789811040856
dc.identifier.issn16800737
dc.identifier.urihttp://hdl.handle.net/11407/4263
dc.description.abstractLead (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.eng
dc.language.isoeng
dc.publisherSpringer Verlagspa
dc.relation.isversionofhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85018384836&doi=10.1007%2f978-981-10-4086-3_17&partnerID=40&md5=5ad5b61b412e38f00f9528d881e9d054spa
dc.sourceScopusspa
dc.titleLead (Pb++) effect on human atrial action potential under normal and atrial fibrillation conditions. In silico studyspa
dc.typeConference Papereng
dc.rights.accessrightsinfo:eu-repo/semantics/restrictedAccess
dc.contributor.affiliationTobón, C., MATBIOM, Universidad de Medellín, Medellín, Colombiaspa
dc.contributor.affiliationPachajoa, D., GI2B, Instituto Tecnológico Metropolitano, Medellín, Colombiaspa
dc.contributor.affiliationUgarte, J.P., Grupo de Dinámica Cardiovascular, Universidad Pontificia Bolivariana, Medellín, Colombiaspa
dc.contributor.affiliationSaiz, J., CI2B, Universitat Politècnica de València, Valencia, Spainspa
dc.identifier.doi10.1007/978-981-10-4086-3_17
dc.subject.keywordAtrial fibrillationeng
dc.subject.keywordIn silico modelseng
dc.subject.keywordL-type Ca++ currenteng
dc.subject.keywordLead (Pb++)eng
dc.subject.keywordBiomedical engineeringeng
dc.subject.keywordCalciumeng
dc.subject.keywordDiseaseseng
dc.subject.keywordElectrophysiologyeng
dc.subject.keywordAction potential durationseng
dc.subject.keywordAction potentialseng
dc.subject.keywordAdverse effecteng
dc.subject.keywordAtrial fibrillationeng
dc.subject.keywordCalcium currenteng
dc.subject.keywordHealthy peopleeng
dc.subject.keywordIn-silico modelseng
dc.subject.keywordToxic agentseng
dc.subject.keywordLeadeng
dc.publisher.facultyFacultad de Ciencias Básicasspa
dc.abstractLead (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.eng
dc.creator.affiliationMATBIOM, Universidad de Medellín, Medellín, Colombiaspa
dc.creator.affiliationGI2B, Instituto Tecnológico Metropolitano, Medellín, Colombiaspa
dc.creator.affiliationGrupo de Dinámica Cardiovascular, Universidad Pontificia Bolivariana, Medellín, Colombiaspa
dc.creator.affiliationCI2B, Universitat Politècnica de València, Valencia, Spainspa
dc.relation.ispartofesIFMBE Proceedingsspa
dc.relation.ispartofesIFMBE Proceedings Volume 60, 2017, Pages 66-69spa
dc.relation.referencesRevealing the costs of air pollution from industrial facilities in europe. (2011). Revealing the Costs of Air Pollution from Industrial Facilities in Europe.spa
dc.relation.referencesAcosta, 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.spa
dc.relation.referencesAnsari, 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.2013.01.024spa
dc.relation.referencesBarbosa 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/s00204-006-0111-3spa
dc.relation.referencesBernal, 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.spa
dc.relation.referencesBhatnagar, A. (2004). Cardiovascular pathophysiology of environmental pollutants. American Journal of Physiology - Heart and Circulatory Physiology, 286(2 55-2), H479-H485.spa
dc.relation.referencesCourtemanche, 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.spa
dc.relation.referencesCourtemanche, 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)00034-6spa
dc.relation.referencesDinanian, 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/ehn140spa
dc.relation.referencesGoralnick, E., & Bontempo, L. J. (2015). Atrial fibrillation. Emergency Medicine Clinics of North America, 33(3), 597-612. doi:10.1016/j.emc.2015.04.008spa
dc.relation.referencesKopp, 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)90093-5spa
dc.relation.referencesPatrick, 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.spa
dc.relation.referencesPrentice, 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-Xspa
dc.relation.referencesRodrigue, J. P. (2013). Pollutants emitted by transport systems (air, water and noise). Pollutants Emitted by Transport Systems (Air, Water and Noise).spa
dc.relation.referencesTsao, 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.1999.8871spa
dc.relation.referencesVan Wagoner, D. R. (2003). Electrophysiological remodeling in human atrial fibrillation. PACE - Pacing and Clinical Electrophysiology, 26(7 II), 1572-1575.spa
dc.relation.referencesVan 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.spa
dc.relation.referencesVaziri, 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.xspa
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dc.type.driverinfo:eu-repo/semantics/conferenceObject
dc.identifier.reponamereponame:Repositorio Institucional Universidad de Medellínspa
dc.identifier.instnameinstname:Universidad de Medellínspa


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