{"database":"BioModels","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Pdf":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017.pdf"],"Owl":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017-biopax2.owl","https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017-biopax3.owl"],"Svg":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017.svg"],"Xml":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017_urn.xml","https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017_url.xml"],"Other":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017.m","https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017.sci","https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017.png","https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017.xpp","https://www.ebi.ac.uk/biomodels/model/download/MODEL1006230017?filename=MODEL1006230017.vcml"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"submitter":["Camille Laibe"],"curationStatus":["Non-curated"],"modellingApproach":["ordinary differential equation model"],"levelVersion":["L2V4"],"full_dataset_link":["https://www.ebi.ac.uk/biomodels/MODEL1006230017"],"publication_pubmed":["19186122"],"isPrivate":["false"],"repository":["BioModels"],"modelFormat":["SBML"],"omics_type":["Models"],"tokenised_name":["Aslanidi2009 RightAtrialTissue Arrhythmogenesis"],"publication_year":["2009"],"submissionId":["MODEL1006230017"],"publication_authors":["Oleg V Aslanidi, Mark R Boyett, Halina Dobrzynski, Jue Li, Henggui Zhang"],"first_author":["Oleg V Aslanidi"],"publication":["19186122,\n                            Experimental evidence suggests that regional differences in action potential (AP) morphology can provide a substrate for initiation and maintenance of reentrant arrhythmias in the right atrium (RA), but the relationships between the complex electrophysiological and anatomical organization of the RA and the genesis of reentry are unclear. In this study, a biophysically detailed three-dimensional computer model of the right atrial tissue was constructed to study the role of tissue heterogeneity and anisotropy in arrhythmogenesis. The model of Lindblad et al. for a rabbit atrial cell was modified to incorporate experimental data on regional differences in several ionic currents (primarily, I(Na), I(CaL), I(K1), I(to), and I(sus)) between the crista terminalis and pectinate muscle cells. The modified model was validated by its ability to reproduce the AP properties measured experimentally. The anatomical model of the rabbit RA (including tissue geometry and fiber orientation) was based on a recent histological reconstruction. Simulations with the resultant electrophysiologically and anatomically detailed three-dimensional model show that complex organization of the RA tissue causes breakdown of regular AP conduction patterns at high pacing rates (>11.75 Hz): as the AP in the crista terminalis cells is longer, and electrotonic coupling transverse to fibers of the crista terminalis is weak, high-frequency pacing at the border between the crista terminalis and pectinate muscles results in a unidirectional conduction block toward the crista terminalis and generation of reentry. Contributions of the tissue heterogeneity and anisotropy to reentry initiation mechanisms are quantified by measuring action potential duration (APD) gradients at the border between the crista terminalis and pectinate muscles: the APD gradients are high in areas where both heterogeneity and anisotropy are high, such that intrinsic APD differences are not diminished by electrotonic interactions. Thus, our detailed computer model reconstructs complex electrical activity in the RA, and provides new insights into the mechanisms of transition from focal atrial tachycardia into reentry.. 3, 96.\n                            Biological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, United Kingdom."],"submitter_mail":["laibe@ebi.ac.uk"],"submitter_affiliation":["EMBL-EBI"],"pubmed_abstract":["Experimental evidence suggests that regional differences in action potential (AP) morphology can provide a substrate for initiation and maintenance of reentrant arrhythmias in the right atrium (RA), but the relationships between the complex electrophysiological and anatomical organization of the RA and the genesis of reentry are unclear. In this study, a biophysically detailed three-dimensional computer model of the right atrial tissue was constructed to study the role of tissue heterogeneity and anisotropy in arrhythmogenesis. The model of Lindblad et al. for a rabbit atrial cell was modified to incorporate experimental data on regional differences in several ionic currents (primarily, I(Na), I(CaL), I(K1), I(to), and I(sus)) between the crista terminalis and pectinate muscle cells. The modified model was validated by its ability to reproduce the AP properties measured experimentally. The anatomical model of the rabbit RA (including tissue geometry and fiber orientation) was based on a recent histological reconstruction. Simulations with the resultant electrophysiologically and anatomically detailed three-dimensional model show that complex organization of the RA tissue causes breakdown of regular AP conduction patterns at high pacing rates (>11.75 Hz): as the AP in the crista terminalis cells is longer, and electrotonic coupling transverse to fibers of the crista terminalis is weak, high-frequency pacing at the border between the crista terminalis and pectinate muscles results in a unidirectional conduction block toward the crista terminalis and generation of reentry. Contributions of the tissue heterogeneity and anisotropy to reentry initiation mechanisms are quantified by measuring action potential duration (APD) gradients at the border between the crista terminalis and pectinate muscles: the APD gradients are high in areas where both heterogeneity and anisotropy are high, such that intrinsic APD differences are not diminished by electrotonic interactions. Thus, our detailed computer model reconstructs complex electrical activity in the RA, and provides new insights into the mechanisms of transition from focal atrial tachycardia into reentry."],"pubmed_title":["Mechanisms of transition from normal to reentrant electrical activity in a model of rabbit atrial tissue: interaction of tissue heterogeneity and anisotropy."],"pubmed_authors":["Aslanidi Oleg V OV, Boyett Mark R MR, Dobrzynski Halina H, Li Jue J, Zhang Henggui H"],"additional_accession":[]},"is_claimable":false,"name":"Aslanidi2009_RightAtrialTissue_Arrhythmogenesis","description":"\n      \n        This a model from the article:      \n        Mechanisms of transition from normal to reentrant electrical activity in a model\nof rabbit atrial tissue: interaction of tissue heterogeneity and anisotropy.\n        \n          Aslanidi OV, Boyett MR, Dobrzynski H, Li J, Zhang H.      Biophys J\n          2009 Feb;96(3):798-817      19186122\n          ,      \n        Abstract:\n        \n          Experimental evidence suggests that regional differences in action potential\n(AP) morphology can provide a substrate for initiation and maintenance of\nreentrant arrhythmias in the right atrium (RA), but the relationships between\nthe complex electrophysiological and anatomical organization of the RA and the\ngenesis of reentry are unclear. In this study, a biophysically detailed\nthree-dimensional computer model of the right atrial tissue was constructed to\nstudy the role of tissue heterogeneity and anisotropy in arrhythmogenesis. The\nmodel of Lindblad et al. for a rabbit atrial cell was modified to incorporate\nexperimental data on regional differences in several ionic currents (primarily,\nI(Na), I(CaL), I(K1), I(to), and I(sus)) between the crista terminalis and\npectinate muscle cells. The modified model was validated by its ability to\nreproduce the AP properties measured experimentally. The anatomical model of the\nrabbit RA (including tissue geometry and fiber orientation) was based on a\nrecent histological reconstruction. Simulations with the resultant\nelectrophysiologically and anatomically detailed three-dimensional model show\nthat complex organization of the RA tissue causes breakdown of regular AP\nconduction patterns at high pacing rates (>11.75 Hz): as the AP in the crista\nterminalis cells is longer, and electrotonic coupling transverse to fibers of\nthe crista terminalis is weak, high-frequency pacing at the border between the\ncrista terminalis and pectinate muscles results in a unidirectional conduction\nblock toward the crista terminalis and generation of reentry. Contributions of\nthe tissue heterogeneity and anisotropy to reentry initiation mechanisms are\nquantified by measuring action potential duration (APD) gradients at the border\nbetween the crista terminalis and pectinate muscles: the APD gradients are high\nin areas where both heterogeneity and anisotropy are high, such that intrinsic\nAPD differences are not diminished by electrotonic interactions. Thus, our\ndetailed computer model reconstructs complex electrical activity in the RA, and\nprovides new insights into the mechanisms of transition from focal atrial\ntachycardia into reentry.      \n      This model was taken from the      CellML repository\n          and automatically converted to SBML.      \n          The original model was:      \n        Aslanidi OV, Boyett MR, Dobrzynski H, Li J, Zhang H. (2009) - version=1.0\n      \n      \n          The original CellML model was created by:      \n      Penny Noble\n      \n          penny.noble@dpag.ox.ac.uk      \n          The University of Oxford      \n    To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to      CC0 Public Domain Dedication\n          for more information.      \n  In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.\n  To cite BioModels Database, please use:      Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.\n\n\n","dates":{"last_modification":"2012-02-02","publication":"2005-01-01","submission":"2010-06-23"},"accession":"MODEL1006230017","cross_references":{"pubmed":["19186122"],"biomodels__db":["MODEL1006230017"],"go":["GO:0086001"],"taxonomy":["9986"],"bto":["BTO:0002320"]}}