Delayed low pressure at reperfusion: A new approach for cardioprotection.
Identifieur interne : 000055 ( PubMed/Curation ); précédent : 000054; suivant : 000056Delayed low pressure at reperfusion: A new approach for cardioprotection.
Auteurs : René Ferrera [France] ; Souhila Benhabbouche [France] ; Claire Crola Da Silva [France] ; Muhammad Rizwan Alam [France] ; Michel Ovize [France]Source :
- The Journal of thoracic and cardiovascular surgery ; 2015.
English descriptors
- KwdEn :
- MESH :
- chemical : Mitochondrial Membrane Transport Proteins.
- physiology : Blood Pressure.
- prevention & control : Myocardial Reperfusion Injury.
- Animals, Disease Models, Animal, Ischemic Preconditioning, Myocardial, Male, Random Allocation, Rats, Rats, Wistar.
Abstract
The aims of this study were to evaluate whether the delayed application of low-pressure reperfusion could reduce lethal reperfusion injury and whether the inhibition of the opening of the mitochondrial permeability transition pore is involved in this protection.
DOI: 10.1016/j.jtcvs.2015.08.053
PubMed: 26384749
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pubmed:26384749Le document en format XML
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<author><name sortKey="Ferrera, Rene" sort="Ferrera, Rene" uniqKey="Ferrera R" first="René" last="Ferrera">René Ferrera</name>
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<author><name sortKey="Benhabbouche, Souhila" sort="Benhabbouche, Souhila" uniqKey="Benhabbouche S" first="Souhila" last="Benhabbouche">Souhila Benhabbouche</name>
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<author><name sortKey="Alam, Muhammad Rizwan" sort="Alam, Muhammad Rizwan" uniqKey="Alam M" first="Muhammad Rizwan" last="Alam">Muhammad Rizwan Alam</name>
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<author><name sortKey="Ovize, Michel" sort="Ovize, Michel" uniqKey="Ovize M" first="Michel" last="Ovize">Michel Ovize</name>
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<author><name sortKey="Ovize, Michel" sort="Ovize, Michel" uniqKey="Ovize M" first="Michel" last="Ovize">Michel Ovize</name>
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<term>Ischemic Preconditioning, Myocardial</term>
<term>Male</term>
<term>Mitochondrial Membrane Transport Proteins</term>
<term>Myocardial Reperfusion Injury (prevention & control)</term>
<term>Random Allocation</term>
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<term>Disease Models, Animal</term>
<term>Ischemic Preconditioning, Myocardial</term>
<term>Male</term>
<term>Random Allocation</term>
<term>Rats</term>
<term>Rats, Wistar</term>
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<front><div type="abstract" xml:lang="en">The aims of this study were to evaluate whether the delayed application of low-pressure reperfusion could reduce lethal reperfusion injury and whether the inhibition of the opening of the mitochondrial permeability transition pore is involved in this protection.</div>
</front>
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<Title>The Journal of thoracic and cardiovascular surgery</Title>
<ISOAbbreviation>J. Thorac. Cardiovasc. Surg.</ISOAbbreviation>
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<ArticleTitle>Delayed low pressure at reperfusion: A new approach for cardioprotection.</ArticleTitle>
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<Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">The aims of this study were to evaluate whether the delayed application of low-pressure reperfusion could reduce lethal reperfusion injury and whether the inhibition of the opening of the mitochondrial permeability transition pore is involved in this protection.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Isolated rat hearts (n = 120) underwent 40 minutes of global ischemia followed by 60 minutes of reperfusion. Hearts were randomly assigned to the following groups: control, postconditioning (comprising 2 episodes of 30 seconds of ischemia and 30 seconds of reperfusion), and low-pressure reperfusion (using a reduction of perfusion pressure at 70 cm H2O for 10 minutes). In additional groups, postconditioning and low-pressure reperfusion were applied after a delay of 3, 10, and 20 minutes after the initial 40-minute ischemic insult.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">As expected, infarct size (triphenyltetrazolium chloride staining) and lactate dehydrogenase release were significantly reduced in low-pressure reperfusion and postconditioning versus controls (P < .01), whereas functional parameters (coronary flow, rate pressure product) were improved (P < .01). Although delaying postconditioning by more than 3 minutes resulted in a loss of protection, low-pressure reperfusion still significantly reduced infarct size when applied as late as 20 minutes after reperfusion. This delayed low-pressure reperfusion protection was associated with an improved mitochondrial respiration, lower reactive oxygen species production, and enhanced calcium retention capacity, related to inhibition of permeability transition pore opening.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">We demonstrated for the first time that low-pressure reperfusion can reduce lethal myocardial reperfusion injury even when performed 10 to 20 minutes after the initiation of reperfusion.</AbstractText>
<CopyrightInformation>Copyright © 2015 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ferrera</LastName>
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<AffiliationInfo><Affiliation>Université Lyon 1, Lyon, France. Electronic address: rene.ferrera@univ-lyon1.fr.</Affiliation>
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<Author ValidYN="Y"><LastName>Benhabbouche</LastName>
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