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Simulating the extrinsic regulation of the sinoatrial node cells using a unified computational model
The aim of this work is to develop a computational model to study the extrinsic regulation of the heart rate variability (HRV) during sympathetic and/or vagal stimulation. The model here proposed is based on two recent models of the sinoatrial node cell (SANC) action potential and the influence of t...
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Published in: | Biomedical physics & engineering express 2017-05, Vol.3 (3), p.35009 |
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description | The aim of this work is to develop a computational model to study the extrinsic regulation of the heart rate variability (HRV) during sympathetic and/or vagal stimulation. The model here proposed is based on two recent models of the sinoatrial node cell (SANC) action potential and the influence of the autonomic nervous system (ANS) on the activity of ionic channels of SANCs. The HRV was simulated by applying a random frequency stimulation using both a normal and a beta probability density function (PDF) for different ranges of stimulation frequencies. The HRV was then analyzed by computing the scale exponent using detrended fluctuation analysis. We found that our model reproduces the value of the scale exponent observed in healthy humans ( = 1.07 0.05) when simultaneous vagal and sympathetic stimulus (with beta and normal PDFs, respectively) over the frequency range from 0 to 10 Hz are applied. Our model also predicts a Brownian motion behavior when the muscarinic receptors are blocked ( = 1.8) and the white noise behavior when the b-adrenergic receptors are blocked ( = 0.5). Our results shed light on how the ANS regulates the HRV in healthy conditions, where it is not enough to consider only one stimulation pathway with a simple normal PDF. |
doi_str_mv | 10.1088/2057-1976/aa6bff |
format | article |
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The model here proposed is based on two recent models of the sinoatrial node cell (SANC) action potential and the influence of the autonomic nervous system (ANS) on the activity of ionic channels of SANCs. The HRV was simulated by applying a random frequency stimulation using both a normal and a beta probability density function (PDF) for different ranges of stimulation frequencies. The HRV was then analyzed by computing the scale exponent using detrended fluctuation analysis. We found that our model reproduces the value of the scale exponent observed in healthy humans ( = 1.07 0.05) when simultaneous vagal and sympathetic stimulus (with beta and normal PDFs, respectively) over the frequency range from 0 to 10 Hz are applied. Our model also predicts a Brownian motion behavior when the muscarinic receptors are blocked ( = 1.8) and the white noise behavior when the b-adrenergic receptors are blocked ( = 0.5). Our results shed light on how the ANS regulates the HRV in healthy conditions, where it is not enough to consider only one stimulation pathway with a simple normal PDF.</description><identifier>ISSN: 2057-1976</identifier><identifier>EISSN: 2057-1976</identifier><identifier>DOI: 10.1088/2057-1976/aa6bff</identifier><identifier>CODEN: NJOPFM</identifier><language>eng</language><publisher>IOP Publishing</publisher><subject>autonomic nervous system ; cardiac pacemaker ; detrended fluctuation analysis ; heart models ; ionic channels ; scale exponent ; sinoatrial node cell</subject><ispartof>Biomedical physics & engineering express, 2017-05, Vol.3 (3), p.35009</ispartof><rights>2017 IOP Publishing Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c242t-757697505783af4ce284845dff4dac881300ea5699bd18cc95a7221190c86df73</citedby><cites>FETCH-LOGICAL-c242t-757697505783af4ce284845dff4dac881300ea5699bd18cc95a7221190c86df73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Castellanos, N P</creatorcontrib><creatorcontrib>Godinez, R</creatorcontrib><title>Simulating the extrinsic regulation of the sinoatrial node cells using a unified computational model</title><title>Biomedical physics & engineering express</title><addtitle>BPEX</addtitle><addtitle>Biomed. Phys. Eng. Express</addtitle><description>The aim of this work is to develop a computational model to study the extrinsic regulation of the heart rate variability (HRV) during sympathetic and/or vagal stimulation. The model here proposed is based on two recent models of the sinoatrial node cell (SANC) action potential and the influence of the autonomic nervous system (ANS) on the activity of ionic channels of SANCs. The HRV was simulated by applying a random frequency stimulation using both a normal and a beta probability density function (PDF) for different ranges of stimulation frequencies. The HRV was then analyzed by computing the scale exponent using detrended fluctuation analysis. We found that our model reproduces the value of the scale exponent observed in healthy humans ( = 1.07 0.05) when simultaneous vagal and sympathetic stimulus (with beta and normal PDFs, respectively) over the frequency range from 0 to 10 Hz are applied. Our model also predicts a Brownian motion behavior when the muscarinic receptors are blocked ( = 1.8) and the white noise behavior when the b-adrenergic receptors are blocked ( = 0.5). Our results shed light on how the ANS regulates the HRV in healthy conditions, where it is not enough to consider only one stimulation pathway with a simple normal PDF.</description><subject>autonomic nervous system</subject><subject>cardiac pacemaker</subject><subject>detrended fluctuation analysis</subject><subject>heart models</subject><subject>ionic channels</subject><subject>scale exponent</subject><subject>sinoatrial node cell</subject><issn>2057-1976</issn><issn>2057-1976</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp9kM1LAzEQxYMoWGrvHnPz4toku_k6SlErFDyo55Dmo6bsbpbNLtT_3mwr4kFkDjPM-71heABcY3SHkRBLgigvsORsqTXben8GZj-r81_zJViktEcIYUYYk3QG7GtoxloPod3B4cNBdxj60KZgYO92RyG2MPqjlkIbdZZ1DdtoHTSurhMc0-TVcGyDD85CE5tuHI7GDDYZrK_Ahdd1covvPgfvjw9vq3WxeXl6Xt1vCkMqMhScciY5zc-KUvvKOCIqUVHrfWW1EQKXCDlNmZRbi4UxkmpOCMYSGcGs5-UcoNNd08eUeudV14dG958KIzUFpaYk1JSEOgWVLbcnS4id2sexz0-n__CbP_Bt5w6qzIVKipBUnfXlF5NbeYA</recordid><startdate>20170510</startdate><enddate>20170510</enddate><creator>Castellanos, N P</creator><creator>Godinez, R</creator><general>IOP Publishing</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20170510</creationdate><title>Simulating the extrinsic regulation of the sinoatrial node cells using a unified computational model</title><author>Castellanos, N P ; Godinez, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c242t-757697505783af4ce284845dff4dac881300ea5699bd18cc95a7221190c86df73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>autonomic nervous system</topic><topic>cardiac pacemaker</topic><topic>detrended fluctuation analysis</topic><topic>heart models</topic><topic>ionic channels</topic><topic>scale exponent</topic><topic>sinoatrial node cell</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Castellanos, N P</creatorcontrib><creatorcontrib>Godinez, R</creatorcontrib><collection>CrossRef</collection><jtitle>Biomedical physics & engineering express</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Castellanos, N P</au><au>Godinez, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Simulating the extrinsic regulation of the sinoatrial node cells using a unified computational model</atitle><jtitle>Biomedical physics & engineering express</jtitle><stitle>BPEX</stitle><addtitle>Biomed. Phys. Eng. Express</addtitle><date>2017-05-10</date><risdate>2017</risdate><volume>3</volume><issue>3</issue><spage>35009</spage><pages>35009-</pages><issn>2057-1976</issn><eissn>2057-1976</eissn><coden>NJOPFM</coden><abstract>The aim of this work is to develop a computational model to study the extrinsic regulation of the heart rate variability (HRV) during sympathetic and/or vagal stimulation. The model here proposed is based on two recent models of the sinoatrial node cell (SANC) action potential and the influence of the autonomic nervous system (ANS) on the activity of ionic channels of SANCs. The HRV was simulated by applying a random frequency stimulation using both a normal and a beta probability density function (PDF) for different ranges of stimulation frequencies. The HRV was then analyzed by computing the scale exponent using detrended fluctuation analysis. We found that our model reproduces the value of the scale exponent observed in healthy humans ( = 1.07 0.05) when simultaneous vagal and sympathetic stimulus (with beta and normal PDFs, respectively) over the frequency range from 0 to 10 Hz are applied. Our model also predicts a Brownian motion behavior when the muscarinic receptors are blocked ( = 1.8) and the white noise behavior when the b-adrenergic receptors are blocked ( = 0.5). Our results shed light on how the ANS regulates the HRV in healthy conditions, where it is not enough to consider only one stimulation pathway with a simple normal PDF.</abstract><pub>IOP Publishing</pub><doi>10.1088/2057-1976/aa6bff</doi><tpages>13</tpages></addata></record> |
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subjects | autonomic nervous system cardiac pacemaker detrended fluctuation analysis heart models ionic channels scale exponent sinoatrial node cell |
title | Simulating the extrinsic regulation of the sinoatrial node cells using a unified computational model |
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