Uniaxial strain of cultured mouse and rat cardiomyocyte strands slows conduction more when its axis is parallel to impulse propagation than when it is perpendicular

Aim Cardiac tissue deformation can modify tissue resistance, membrane capacitance and ion currents and hence cause arrhythmogenic slow conduction. Our aim was to investigate whether uniaxial strain causes different changes in conduction velocity (θ) when the principal strain axis is parallel vs perp...

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Veröffentlicht in:Acta Physiologica 2018-05, Vol.223 (1), p.e13026-n/a
Hauptverfasser: Buccarello, A., Azzarito, M., Michoud, F., Lacour, S. P., Kucera, J. P.
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creator Buccarello, A.
Azzarito, M.
Michoud, F.
Lacour, S. P.
Kucera, J. P.
description Aim Cardiac tissue deformation can modify tissue resistance, membrane capacitance and ion currents and hence cause arrhythmogenic slow conduction. Our aim was to investigate whether uniaxial strain causes different changes in conduction velocity (θ) when the principal strain axis is parallel vs perpendicular to impulse propagation. Methods Cardiomyocyte strands were cultured on stretchable custom microelectrode arrays, and θ was determined during steady‐state pacing. Uniaxial strain (5%) with principal axis parallel (orthodromic) or perpendicular (paradromic) to propagation was applied for 1 minute and controlled by imaging a grid of markers. The results were analysed in terms of cable theory. Results Both types of strain induced immediate changes of θ upon application and release. In material coordinates, orthodromic strain decreased θ significantly more (P 
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P. ; Kucera, J. P.</creator><creatorcontrib>Buccarello, A. ; Azzarito, M. ; Michoud, F. ; Lacour, S. P. ; Kucera, J. P.</creatorcontrib><description>Aim Cardiac tissue deformation can modify tissue resistance, membrane capacitance and ion currents and hence cause arrhythmogenic slow conduction. Our aim was to investigate whether uniaxial strain causes different changes in conduction velocity (θ) when the principal strain axis is parallel vs perpendicular to impulse propagation. Methods Cardiomyocyte strands were cultured on stretchable custom microelectrode arrays, and θ was determined during steady‐state pacing. Uniaxial strain (5%) with principal axis parallel (orthodromic) or perpendicular (paradromic) to propagation was applied for 1 minute and controlled by imaging a grid of markers. The results were analysed in terms of cable theory. Results Both types of strain induced immediate changes of θ upon application and release. In material coordinates, orthodromic strain decreased θ significantly more (P &lt; .001) than paradromic strain (2.2 ± 0.5% vs 1.0 ± 0.2% in n = 8 mouse cardiomyocyte cultures, 2.3 ± 0.4% vs 0.9 ± 0.5% in n = 4 rat cardiomyocyte cultures, respectively). The larger effect of orthodromic strain can be explained by the increase in axial myoplasmic resistance, which is not altered by paradromic strain. Thus, changes in tissue resistance substantially contributed to the changes of θ during strain, in addition to other influences (eg stretch‐activated channels). Besides these immediate effects, the application of strain also consistently initiated a slow progressive decrease in θ and a slow recovery of θ upon release. Conclusion Changes in cardiac conduction velocity caused by acute stretch do not only depend on the magnitude of strain but also on its orientation relative to impulse propagation. This dependence is due to different effects on tissue resistance.</description><identifier>ISSN: 1748-1708</identifier><identifier>EISSN: 1748-1716</identifier><identifier>DOI: 10.1111/apha.13026</identifier><identifier>PMID: 29282897</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>cable theory ; cardiac action potential ; cardiac cell cultures ; Cardiomyocytes ; Conduction ; conduction velocity ; Heart ; Heart diseases ; Ion currents ; mechano‐electrical feedback ; Membrane capacitance ; Propagation ; stretchable microelectrode arrays ; Velocity</subject><ispartof>Acta Physiologica, 2018-05, Vol.223 (1), p.e13026-n/a</ispartof><rights>2017 Scandinavian Physiological Society. Published by John Wiley &amp; Sons Ltd</rights><rights>2017 Scandinavian Physiological Society. 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P.</creatorcontrib><creatorcontrib>Kucera, J. P.</creatorcontrib><title>Uniaxial strain of cultured mouse and rat cardiomyocyte strands slows conduction more when its axis is parallel to impulse propagation than when it is perpendicular</title><title>Acta Physiologica</title><addtitle>Acta Physiol (Oxf)</addtitle><description>Aim Cardiac tissue deformation can modify tissue resistance, membrane capacitance and ion currents and hence cause arrhythmogenic slow conduction. Our aim was to investigate whether uniaxial strain causes different changes in conduction velocity (θ) when the principal strain axis is parallel vs perpendicular to impulse propagation. Methods Cardiomyocyte strands were cultured on stretchable custom microelectrode arrays, and θ was determined during steady‐state pacing. Uniaxial strain (5%) with principal axis parallel (orthodromic) or perpendicular (paradromic) to propagation was applied for 1 minute and controlled by imaging a grid of markers. The results were analysed in terms of cable theory. Results Both types of strain induced immediate changes of θ upon application and release. In material coordinates, orthodromic strain decreased θ significantly more (P &lt; .001) than paradromic strain (2.2 ± 0.5% vs 1.0 ± 0.2% in n = 8 mouse cardiomyocyte cultures, 2.3 ± 0.4% vs 0.9 ± 0.5% in n = 4 rat cardiomyocyte cultures, respectively). The larger effect of orthodromic strain can be explained by the increase in axial myoplasmic resistance, which is not altered by paradromic strain. Thus, changes in tissue resistance substantially contributed to the changes of θ during strain, in addition to other influences (eg stretch‐activated channels). Besides these immediate effects, the application of strain also consistently initiated a slow progressive decrease in θ and a slow recovery of θ upon release. Conclusion Changes in cardiac conduction velocity caused by acute stretch do not only depend on the magnitude of strain but also on its orientation relative to impulse propagation. This dependence is due to different effects on tissue resistance.</description><subject>cable theory</subject><subject>cardiac action potential</subject><subject>cardiac cell cultures</subject><subject>Cardiomyocytes</subject><subject>Conduction</subject><subject>conduction velocity</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Ion currents</subject><subject>mechano‐electrical feedback</subject><subject>Membrane capacitance</subject><subject>Propagation</subject><subject>stretchable microelectrode arrays</subject><subject>Velocity</subject><issn>1748-1708</issn><issn>1748-1716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9kc1KJDEUhYOMjOK4mQcYAm5EaCc_VZXUshFHBwRd6DrcSqXsSCqpSVK0_T4-6KS71cUsJgRyF98595CD0HdKLmk5P2FawSXlhDUH6JiKSi6ooM2Xz5nII3Sa0gshhDLKK8a-oiPWMslkK47R25O38GrB4ZQjWI_DgPXs8hxNj8cwJ4PB9zhCxhpib8O4CXqTzQ73fcLJhXXCOvh-1tkGX0TR4PXKeGxzwsU74XIniOCccTgHbMdpdsV4imGCZ9ip8gr8h2rHmzgZ39uSBeI3dDhAUZy-vyfo6df149Xt4u7-5vfV8m6hecubRUNI3fCqZoNoBzkQxhspGW0rrkGKCnRLm64eZE-6uiZEdJzQjtWik0NjTG34CTrf-5Zkf2aTshpt0sY58KZ8haKtpKKsElVBz_5BX8IcfUmnWFksKWEVL9TFntIxpBTNoKZoR4gbRYna1qe29aldfQX-8W45d6PpP9GPsgpA98DaOrP5j5VaPtwu96Z_Abrjpuc</recordid><startdate>201805</startdate><enddate>201805</enddate><creator>Buccarello, A.</creator><creator>Azzarito, M.</creator><creator>Michoud, F.</creator><creator>Lacour, S. P.</creator><creator>Kucera, J. P.</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7TS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9190-8599</orcidid><orcidid>https://orcid.org/0000-0001-9075-4022</orcidid><orcidid>https://orcid.org/0000-0003-0310-6962</orcidid></search><sort><creationdate>201805</creationdate><title>Uniaxial strain of cultured mouse and rat cardiomyocyte strands slows conduction more when its axis is parallel to impulse propagation than when it is perpendicular</title><author>Buccarello, A. ; Azzarito, M. ; Michoud, F. ; Lacour, S. P. ; Kucera, J. P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3936-600563452f79f8f02368821943ca874ac916b5f8d0b55007b301b257b8f6ee5e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>cable theory</topic><topic>cardiac action potential</topic><topic>cardiac cell cultures</topic><topic>Cardiomyocytes</topic><topic>Conduction</topic><topic>conduction velocity</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Ion currents</topic><topic>mechano‐electrical feedback</topic><topic>Membrane capacitance</topic><topic>Propagation</topic><topic>stretchable microelectrode arrays</topic><topic>Velocity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Buccarello, A.</creatorcontrib><creatorcontrib>Azzarito, M.</creatorcontrib><creatorcontrib>Michoud, F.</creatorcontrib><creatorcontrib>Lacour, S. P.</creatorcontrib><creatorcontrib>Kucera, J. P.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>MEDLINE - Academic</collection><jtitle>Acta Physiologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Buccarello, A.</au><au>Azzarito, M.</au><au>Michoud, F.</au><au>Lacour, S. P.</au><au>Kucera, J. P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Uniaxial strain of cultured mouse and rat cardiomyocyte strands slows conduction more when its axis is parallel to impulse propagation than when it is perpendicular</atitle><jtitle>Acta Physiologica</jtitle><addtitle>Acta Physiol (Oxf)</addtitle><date>2018-05</date><risdate>2018</risdate><volume>223</volume><issue>1</issue><spage>e13026</spage><epage>n/a</epage><pages>e13026-n/a</pages><issn>1748-1708</issn><eissn>1748-1716</eissn><abstract>Aim Cardiac tissue deformation can modify tissue resistance, membrane capacitance and ion currents and hence cause arrhythmogenic slow conduction. Our aim was to investigate whether uniaxial strain causes different changes in conduction velocity (θ) when the principal strain axis is parallel vs perpendicular to impulse propagation. Methods Cardiomyocyte strands were cultured on stretchable custom microelectrode arrays, and θ was determined during steady‐state pacing. Uniaxial strain (5%) with principal axis parallel (orthodromic) or perpendicular (paradromic) to propagation was applied for 1 minute and controlled by imaging a grid of markers. The results were analysed in terms of cable theory. Results Both types of strain induced immediate changes of θ upon application and release. In material coordinates, orthodromic strain decreased θ significantly more (P &lt; .001) than paradromic strain (2.2 ± 0.5% vs 1.0 ± 0.2% in n = 8 mouse cardiomyocyte cultures, 2.3 ± 0.4% vs 0.9 ± 0.5% in n = 4 rat cardiomyocyte cultures, respectively). The larger effect of orthodromic strain can be explained by the increase in axial myoplasmic resistance, which is not altered by paradromic strain. Thus, changes in tissue resistance substantially contributed to the changes of θ during strain, in addition to other influences (eg stretch‐activated channels). Besides these immediate effects, the application of strain also consistently initiated a slow progressive decrease in θ and a slow recovery of θ upon release. Conclusion Changes in cardiac conduction velocity caused by acute stretch do not only depend on the magnitude of strain but also on its orientation relative to impulse propagation. This dependence is due to different effects on tissue resistance.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29282897</pmid><doi>10.1111/apha.13026</doi><tpages>19</tpages><orcidid>https://orcid.org/0000-0001-9190-8599</orcidid><orcidid>https://orcid.org/0000-0001-9075-4022</orcidid><orcidid>https://orcid.org/0000-0003-0310-6962</orcidid><oa>free_for_read</oa></addata></record>
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subjects cable theory
cardiac action potential
cardiac cell cultures
Cardiomyocytes
Conduction
conduction velocity
Heart
Heart diseases
Ion currents
mechano‐electrical feedback
Membrane capacitance
Propagation
stretchable microelectrode arrays
Velocity
title Uniaxial strain of cultured mouse and rat cardiomyocyte strands slows conduction more when its axis is parallel to impulse propagation than when it is perpendicular
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