Systems approach to the study of stretch and arrhythmias in right ventricular failure induced in rats by monocrotaline
Identifieur interne : 003482 ( Main/Exploration ); précédent : 003481; suivant : 003483Systems approach to the study of stretch and arrhythmias in right ventricular failure induced in rats by monocrotaline
Auteurs : David Benoist [Royaume-Uni, France] ; Rachel Stones [Royaume-Uni] ; Alan P. Benson [Royaume-Uni] ; Ewan D. Fowler [Royaume-Uni] ; Mark J. Drinkhill [Royaume-Uni] ; Matthew E. L. Hardy [Royaume-Uni] ; David A. Saint [Australie] ; Olivier Cazorla [France] ; Olivier Bernus [Royaume-Uni, France] ; Ed White [Royaume-Uni]Source :
- Progress in Biophysics and Molecular Biology [ 0079-6107 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Biologie des systèmes (), Canaux ioniques (métabolisme), Contrainte mécanique, Couplage excitation-contraction, Dysfonction ventriculaire droite (), Dysfonction ventriculaire droite (physiopathologie), Hypertension pulmonaire (), Hypertension pulmonaire (physiopathologie), Module d'élasticité, Monocrotaline, Mécanotransduction cellulaire, Ouverture et fermeture des portes des canaux ioniques, Rat Wistar, Rats, Remodelage ventriculaire, Stimulation physique (), Système de conduction du coeur (), Système de conduction du coeur (physiopathologie), Troubles du rythme cardiaque (), Troubles du rythme cardiaque (physiopathologie).
- MESH :
- métabolisme : Canaux ioniques.
- physiopathologie : Dysfonction ventriculaire droite, Hypertension pulmonaire, Système de conduction du coeur, Troubles du rythme cardiaque.
- Animaux, Biologie des systèmes, Contrainte mécanique, Couplage excitation-contraction, Dysfonction ventriculaire droite, Hypertension pulmonaire, Module d'élasticité, Monocrotaline, Mécanotransduction cellulaire, Ouverture et fermeture des portes des canaux ioniques, Rat Wistar, Rats, Remodelage ventriculaire, Stimulation physique, Système de conduction du coeur, Troubles du rythme cardiaque.
English descriptors
- KwdEn :
- Animals, Arrhythmias, Cardiac (chemically induced), Arrhythmias, Cardiac (physiopathology), Elastic Modulus, Excitation Contraction Coupling, Heart Conduction System (drug effects), Heart Conduction System (physiopathology), Hypertension, Pulmonary (chemically induced), Hypertension, Pulmonary (physiopathology), Ion Channel Gating, Ion Channels (metabolism), Mechanotransduction, Cellular, Monocrotaline, Physical Stimulation (methods), Rats, Rats, Wistar, Stress, Mechanical, Systems Biology (methods), Ventricular Dysfunction, Right (chemically induced), Ventricular Dysfunction, Right (physiopathology), Ventricular Remodeling.
- MESH :
- chemical , metabolism : Ion Channels.
- chemically induced : Arrhythmias, Cardiac, Hypertension, Pulmonary, Ventricular Dysfunction, Right.
- drug effects : Heart Conduction System.
- methods : Physical Stimulation, Systems Biology.
- physiopathology : Arrhythmias, Cardiac, Heart Conduction System, Hypertension, Pulmonary, Ventricular Dysfunction, Right.
- Animals, Elastic Modulus, Excitation Contraction Coupling, Ion Channel Gating, Mechanotransduction, Cellular, Monocrotaline, Rats, Rats, Wistar, Stress, Mechanical, Ventricular Remodeling.
Abstract
We demonstrate the synergistic benefits of using multiple technologies to investigate complex multi-scale biological responses. The combination of reductionist and integrative methodologies can reveal novel insights into mechanisms of action by tracking changes of
We show arrhythmogenic T-wave alternans in the ECG of conscious heart failure animals. Optical mapping of isolated hearts revealed discordant action potential duration (APD) alternans. Potential causes of the arrhythmic substrate; structural remodelling and/or steep APD restitution and dispersion were observed, with specific remodelling of the Right Ventricular Outflow Tract. At the myocyte level, [Ca2+]i transient alternans were observed together with decreased activity, gene and protein expression of the sarcoplasmic reticulum Ca2+-ATPase (SERCA). Computer simulations of the electrical and structural remodelling suggest both contribute to a less stable substrate.
Echocardiography was used to estimate increased wall stress in failure,
Url:
DOI: 10.1016/j.pbiomolbio.2014.06.008
PubMed: 25016242
PubMed Central: 4210667
Affiliations:
- Australie, France, Royaume-Uni
- Angleterre, Aquitaine, Grand Manchester, Languedoc-Roussillon, Nouvelle-Aquitaine, Occitanie (région administrative), Yorkshire-et-Humber
- Bordeaux, Leeds, Manchester, Montpellier
- PRES Sud de France, Université Montpellier 2, Université de Bordeaux, Université de Leeds, Université de Manchester
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Le document en format XML
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<series><title level="j">Progress in Biophysics and Molecular Biology</title>
<idno type="ISSN">0079-6107</idno>
<idno type="eISSN">1873-1732</idno>
<imprint><date when="2014">2014</date>
</imprint>
</series>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Arrhythmias, Cardiac (chemically induced)</term>
<term>Arrhythmias, Cardiac (physiopathology)</term>
<term>Elastic Modulus</term>
<term>Excitation Contraction Coupling</term>
<term>Heart Conduction System (drug effects)</term>
<term>Heart Conduction System (physiopathology)</term>
<term>Hypertension, Pulmonary (chemically induced)</term>
<term>Hypertension, Pulmonary (physiopathology)</term>
<term>Ion Channel Gating</term>
<term>Ion Channels (metabolism)</term>
<term>Mechanotransduction, Cellular</term>
<term>Monocrotaline</term>
<term>Physical Stimulation (methods)</term>
<term>Rats</term>
<term>Rats, Wistar</term>
<term>Stress, Mechanical</term>
<term>Systems Biology (methods)</term>
<term>Ventricular Dysfunction, Right (chemically induced)</term>
<term>Ventricular Dysfunction, Right (physiopathology)</term>
<term>Ventricular Remodeling</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Biologie des systèmes ()</term>
<term>Canaux ioniques (métabolisme)</term>
<term>Contrainte mécanique</term>
<term>Couplage excitation-contraction</term>
<term>Dysfonction ventriculaire droite ()</term>
<term>Dysfonction ventriculaire droite (physiopathologie)</term>
<term>Hypertension pulmonaire ()</term>
<term>Hypertension pulmonaire (physiopathologie)</term>
<term>Module d'élasticité</term>
<term>Monocrotaline</term>
<term>Mécanotransduction cellulaire</term>
<term>Ouverture et fermeture des portes des canaux ioniques</term>
<term>Rat Wistar</term>
<term>Rats</term>
<term>Remodelage ventriculaire</term>
<term>Stimulation physique ()</term>
<term>Système de conduction du coeur ()</term>
<term>Système de conduction du coeur (physiopathologie)</term>
<term>Troubles du rythme cardiaque ()</term>
<term>Troubles du rythme cardiaque (physiopathologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Ion Channels</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Arrhythmias, Cardiac</term>
<term>Hypertension, Pulmonary</term>
<term>Ventricular Dysfunction, Right</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Heart Conduction System</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Physical Stimulation</term>
<term>Systems Biology</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Canaux ioniques</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Dysfonction ventriculaire droite</term>
<term>Hypertension pulmonaire</term>
<term>Système de conduction du coeur</term>
<term>Troubles du rythme cardiaque</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Arrhythmias, Cardiac</term>
<term>Heart Conduction System</term>
<term>Hypertension, Pulmonary</term>
<term>Ventricular Dysfunction, Right</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Elastic Modulus</term>
<term>Excitation Contraction Coupling</term>
<term>Ion Channel Gating</term>
<term>Mechanotransduction, Cellular</term>
<term>Monocrotaline</term>
<term>Rats</term>
<term>Rats, Wistar</term>
<term>Stress, Mechanical</term>
<term>Ventricular Remodeling</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Biologie des systèmes</term>
<term>Contrainte mécanique</term>
<term>Couplage excitation-contraction</term>
<term>Dysfonction ventriculaire droite</term>
<term>Hypertension pulmonaire</term>
<term>Module d'élasticité</term>
<term>Monocrotaline</term>
<term>Mécanotransduction cellulaire</term>
<term>Ouverture et fermeture des portes des canaux ioniques</term>
<term>Rat Wistar</term>
<term>Rats</term>
<term>Remodelage ventriculaire</term>
<term>Stimulation physique</term>
<term>Système de conduction du coeur</term>
<term>Troubles du rythme cardiaque</term>
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<front><div type="abstract" xml:lang="en"><p>We demonstrate the synergistic benefits of using multiple technologies to investigate complex multi-scale biological responses. The combination of reductionist and integrative methodologies can reveal novel insights into mechanisms of action by tracking changes of <italic>in vivo</italic>
phenomena to alterations in protein activity (or <italic>vice versa</italic>
). We have applied this approach to electrical and mechanical remodelling in right ventricular failure caused by monocrotaline-induced pulmonary artery hypertension in rats.</p>
<p>We show arrhythmogenic T-wave alternans in the ECG of conscious heart failure animals. Optical mapping of isolated hearts revealed discordant action potential duration (APD) alternans. Potential causes of the arrhythmic substrate; structural remodelling and/or steep APD restitution and dispersion were observed, with specific remodelling of the Right Ventricular Outflow Tract. At the myocyte level, [Ca<sup>2+</sup>
]i transient alternans were observed together with decreased activity, gene and protein expression of the sarcoplasmic reticulum Ca<sup>2+</sup>
-ATPase (SERCA). Computer simulations of the electrical and structural remodelling suggest both contribute to a less stable substrate.</p>
<p>Echocardiography was used to estimate increased wall stress in failure, <italic>in vivo</italic>
. Stretch of intact and skinned single myocytes revealed no effect on the Frank-Starling mechanism in failing myocytes. In isolated hearts acute stretch-induced arrhythmias occurred in all preparations. Significant shortening of the early APD was seen in control but not failing hearts. These observations may be linked to changes in the gene expression of candidate mechanosensitive ion channels (MSCs) TREK-1 and TRPC1/6. Computer simulations incorporating MSCs and changes in ion channels with failure, based on altered gene expression, largely reproduced experimental observations.</p>
</div>
</front>
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</TEI>
<affiliations><list><country><li>Australie</li>
<li>France</li>
<li>Royaume-Uni</li>
</country>
<region><li>Angleterre</li>
<li>Aquitaine</li>
<li>Grand Manchester</li>
<li>Languedoc-Roussillon</li>
<li>Nouvelle-Aquitaine</li>
<li>Occitanie (région administrative)</li>
<li>Yorkshire-et-Humber</li>
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<settlement><li>Bordeaux</li>
<li>Leeds</li>
<li>Manchester</li>
<li>Montpellier</li>
</settlement>
<orgName><li>PRES Sud de France</li>
<li>Université Montpellier 2</li>
<li>Université de Bordeaux</li>
<li>Université de Leeds</li>
<li>Université de Manchester</li>
</orgName>
</list>
<tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Benoist, David" sort="Benoist, David" uniqKey="Benoist D" first="David" last="Benoist">David Benoist</name>
</region>
<name sortKey="Benson, Alan P" sort="Benson, Alan P" uniqKey="Benson A" first="Alan P." last="Benson">Alan P. Benson</name>
<name sortKey="Bernus, Olivier" sort="Bernus, Olivier" uniqKey="Bernus O" first="Olivier" last="Bernus">Olivier Bernus</name>
<name sortKey="Drinkhill, Mark J" sort="Drinkhill, Mark J" uniqKey="Drinkhill M" first="Mark J." last="Drinkhill">Mark J. Drinkhill</name>
<name sortKey="Fowler, Ewan D" sort="Fowler, Ewan D" uniqKey="Fowler E" first="Ewan D." last="Fowler">Ewan D. Fowler</name>
<name sortKey="Hardy, Matthew E L" sort="Hardy, Matthew E L" uniqKey="Hardy M" first="Matthew E. L." last="Hardy">Matthew E. L. Hardy</name>
<name sortKey="Hardy, Matthew E L" sort="Hardy, Matthew E L" uniqKey="Hardy M" first="Matthew E. L." last="Hardy">Matthew E. L. Hardy</name>
<name sortKey="Stones, Rachel" sort="Stones, Rachel" uniqKey="Stones R" first="Rachel" last="Stones">Rachel Stones</name>
<name sortKey="White, Ed" sort="White, Ed" uniqKey="White E" first="Ed" last="White">Ed White</name>
</country>
<country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Benoist, David" sort="Benoist, David" uniqKey="Benoist D" first="David" last="Benoist">David Benoist</name>
</region>
<name sortKey="Bernus, Olivier" sort="Bernus, Olivier" uniqKey="Bernus O" first="Olivier" last="Bernus">Olivier Bernus</name>
<name sortKey="Cazorla, Olivier" sort="Cazorla, Olivier" uniqKey="Cazorla O" first="Olivier" last="Cazorla">Olivier Cazorla</name>
</country>
<country name="Australie"><noRegion><name sortKey="Saint, David A" sort="Saint, David A" uniqKey="Saint D" first="David A." last="Saint">David A. Saint</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>
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