Sympathetic nervous response to ischemia-reperfusion injury in humans is altered with remote ischemic preconditioning.
Identifieur interne : 001625 ( PubMed/Checkpoint ); précédent : 001624; suivant : 001626Sympathetic nervous response to ischemia-reperfusion injury in humans is altered with remote ischemic preconditioning.
Auteurs : Elisabeth A. Lambert [Australie] ; Colleen J. Thomas [Australie] ; Robyn Hemmes [Australie] ; Nina Eikelis [Australie] ; Atul Pathak [France] ; Markus P. Schlaich [Australie] ; Gavin W. Lambert [Australie]Source :
- American journal of physiology. Heart and circulatory physiology [ 1522-1539 ] ; 2016.
Descripteurs français
- KwdFr :
- Adolescent, Adulte, Avant-bras, Doigts (), Femelle, Glutathion (sang), Humains, Hyperhémie (physiopathologie), Hyperhémie (sang), Jeune adulte, Lésion d'ischémie-reperfusion (physiopathologie), Lésion d'ischémie-reperfusion (sang), Monoxyde d'azote (sang), Muscles squelettiques (innervation), Mâle, Pléthysmographie, Préconditionnement ischémique, Stress oxydatif, Système nerveux sympathique (physiopathologie), Volontaires sains.
- MESH :
- physiopathologie : Hyperhémie, Lésion d'ischémie-reperfusion, Système nerveux sympathique.
- sang : Glutathion, Hyperhémie, Lésion d'ischémie-reperfusion, Monoxyde d'azote, Muscles squelettiques.
- Adolescent, Adulte, Avant-bras, Doigts, Femelle, Humains, Jeune adulte, Mâle, Pléthysmographie, Préconditionnement ischémique, Stress oxydatif, Volontaires sains.
English descriptors
- KwdEn :
- Adolescent, Adult, Female, Fingers (blood supply), Forearm, Glutathione (blood), Healthy Volunteers, Humans, Hyperemia (blood), Hyperemia (physiopathology), Ischemic Preconditioning, Male, Muscle, Skeletal (innervation), Nitric Oxide (blood), Oxidative Stress, Plethysmography, Reperfusion Injury (blood), Reperfusion Injury (physiopathology), Sympathetic Nervous System (physiopathology), Young Adult.
- MESH :
- chemical , blood : Glutathione, Nitric Oxide.
- blood : Hyperemia, Reperfusion Injury.
- blood supply : Fingers.
- innervation : Muscle, Skeletal.
- physiopathology : Hyperemia, Reperfusion Injury, Sympathetic Nervous System.
- Adolescent, Adult, Female, Forearm, Healthy Volunteers, Humans, Ischemic Preconditioning, Male, Oxidative Stress, Plethysmography, Young Adult.
Abstract
Sympathetic neural activation may be detrimentally involved in tissue injury caused by ischemia-reperfusion (IR). We examined the effects of experimental IR in the forearm on sympathetic nerve response, finger reactive hyperemia, and oxidative stress, and the protection afforded by applying remote ischemic preconditioning (RIPC). Ischemia was induced in the forearm for 20 min in healthy volunteers. RIPC was induced by applying two cycles, 5 min each, of ischemia and reperfusion to the upper leg immediately before IR. We examined muscle sympathetic nerve activity (MSNA) in the contralateral leg using microneurography, finger reactive hyperemia [ischemic reactive hyperemia index (RHI)], erythrocyte production of reduced gluthathione (GSH), and plasma nitric oxide (NO) concentration. In controls (no RIPC; n = 15), IR increased MSNA in the early and late phase of ischemia (70% at 5 min; 101% at 15 min). In subjects who underwent RIPC (n = 15), the increase in MSNA was delayed to the late phase of ischemia and increased only by 40%. GSH increased during ischemia in the control group (P = 0.05), but not in those who underwent RIPC. Nitrate and nitrite concentration, taken as an index of NO availability, decreased during the reperfusion period in control individuals (P < 0.05), while no change was observed in those who underwent RIPC. Experimental IR did not affect RHI in the control condition, but a significant vasodilatory response occurred in the RIPC group (P < 0.05). RIPC attenuated ischemia-induced sympathetic activation, prevented the production of an erythrocyte marker of oxidative stress and the reduction of NO availability, and ameliorated RHI.
DOI: 10.1152/ajpheart.00369.2016
PubMed: 27288436
Affiliations:
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Lambert</name><affiliation wicri:level="1"><nlm:affiliation>Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia; Department of Physiology, Monash University, Clayton, Victoria, Australia; and elisabeth.lambert@bakeridi.edu.au.</nlm:affiliation><country wicri:rule="url">Australie</country><wicri:regionArea>Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia; Department of Physiology, Monash University, Clayton, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Thomas, Colleen J" sort="Thomas, Colleen J" uniqKey="Thomas C" first="Colleen J" last="Thomas">Colleen J. 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Lambert</name><affiliation wicri:level="1"><nlm:affiliation>Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia; Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Victoria, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia; Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author></analytic><series><title level="j">American journal of physiology. Heart and circulatory physiology</title><idno type="eISSN">1522-1539</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Female</term><term>Fingers (blood supply)</term><term>Forearm</term><term>Glutathione (blood)</term><term>Healthy Volunteers</term><term>Humans</term><term>Hyperemia (blood)</term><term>Hyperemia (physiopathology)</term><term>Ischemic Preconditioning</term><term>Male</term><term>Muscle, Skeletal (innervation)</term><term>Nitric Oxide (blood)</term><term>Oxidative Stress</term><term>Plethysmography</term><term>Reperfusion Injury (blood)</term><term>Reperfusion Injury (physiopathology)</term><term>Sympathetic Nervous System (physiopathology)</term><term>Young Adult</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Avant-bras</term><term>Doigts ()</term><term>Femelle</term><term>Glutathion (sang)</term><term>Humains</term><term>Hyperhémie (physiopathologie)</term><term>Hyperhémie (sang)</term><term>Jeune adulte</term><term>Lésion d'ischémie-reperfusion (physiopathologie)</term><term>Lésion d'ischémie-reperfusion (sang)</term><term>Monoxyde d'azote (sang)</term><term>Muscles squelettiques (innervation)</term><term>Mâle</term><term>Pléthysmographie</term><term>Préconditionnement ischémique</term><term>Stress oxydatif</term><term>Système nerveux sympathique (physiopathologie)</term><term>Volontaires sains</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Glutathione</term><term>Nitric Oxide</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Hyperemia</term><term>Reperfusion Injury</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Fingers</term></keywords><keywords scheme="MESH" qualifier="innervation" xml:lang="en"><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Hyperhémie</term><term>Lésion d'ischémie-reperfusion</term><term>Système nerveux sympathique</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hyperemia</term><term>Reperfusion Injury</term><term>Sympathetic Nervous System</term></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Glutathion</term><term>Hyperhémie</term><term>Lésion d'ischémie-reperfusion</term><term>Monoxyde d'azote</term><term>Muscles squelettiques</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Female</term><term>Forearm</term><term>Healthy Volunteers</term><term>Humans</term><term>Ischemic Preconditioning</term><term>Male</term><term>Oxidative Stress</term><term>Plethysmography</term><term>Young Adult</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Avant-bras</term><term>Doigts</term><term>Femelle</term><term>Humains</term><term>Jeune adulte</term><term>Mâle</term><term>Pléthysmographie</term><term>Préconditionnement ischémique</term><term>Stress oxydatif</term><term>Volontaires sains</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Sympathetic neural activation may be detrimentally involved in tissue injury caused by ischemia-reperfusion (IR). We examined the effects of experimental IR in the forearm on sympathetic nerve response, finger reactive hyperemia, and oxidative stress, and the protection afforded by applying remote ischemic preconditioning (RIPC). Ischemia was induced in the forearm for 20 min in healthy volunteers. RIPC was induced by applying two cycles, 5 min each, of ischemia and reperfusion to the upper leg immediately before IR. We examined muscle sympathetic nerve activity (MSNA) in the contralateral leg using microneurography, finger reactive hyperemia [ischemic reactive hyperemia index (RHI)], erythrocyte production of reduced gluthathione (GSH), and plasma nitric oxide (NO) concentration. In controls (no RIPC; n = 15), IR increased MSNA in the early and late phase of ischemia (70% at 5 min; 101% at 15 min). In subjects who underwent RIPC (n = 15), the increase in MSNA was delayed to the late phase of ischemia and increased only by 40%. GSH increased during ischemia in the control group (P = 0.05), but not in those who underwent RIPC. Nitrate and nitrite concentration, taken as an index of NO availability, decreased during the reperfusion period in control individuals (P < 0.05), while no change was observed in those who underwent RIPC. Experimental IR did not affect RHI in the control condition, but a significant vasodilatory response occurred in the RIPC group (P < 0.05). RIPC attenuated ischemia-induced sympathetic activation, prevented the production of an erythrocyte marker of oxidative stress and the reduction of NO availability, and ameliorated RHI.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27288436</PMID><DateCreated><Year>2016</Year><Month>08</Month><Day>02</Day></DateCreated><DateCompleted><Year>2017</Year><Month>06</Month><Day>26</Day></DateCompleted><DateRevised><Year>2017</Year><Month>06</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-1539</ISSN><JournalIssue CitedMedium="Internet"><Volume>311</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>Aug</Month><Day>01</Day></PubDate></JournalIssue><Title>American journal of physiology. Heart and circulatory physiology</Title><ISOAbbreviation>Am. J. Physiol. Heart Circ. Physiol.</ISOAbbreviation></Journal><ArticleTitle>Sympathetic nervous response to ischemia-reperfusion injury in humans is altered with remote ischemic preconditioning.</ArticleTitle><Pagination><MedlinePgn>H364-70</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajpheart.00369.2016</ELocationID><Abstract><AbstractText>Sympathetic neural activation may be detrimentally involved in tissue injury caused by ischemia-reperfusion (IR). We examined the effects of experimental IR in the forearm on sympathetic nerve response, finger reactive hyperemia, and oxidative stress, and the protection afforded by applying remote ischemic preconditioning (RIPC). Ischemia was induced in the forearm for 20 min in healthy volunteers. RIPC was induced by applying two cycles, 5 min each, of ischemia and reperfusion to the upper leg immediately before IR. We examined muscle sympathetic nerve activity (MSNA) in the contralateral leg using microneurography, finger reactive hyperemia [ischemic reactive hyperemia index (RHI)], erythrocyte production of reduced gluthathione (GSH), and plasma nitric oxide (NO) concentration. In controls (no RIPC; n = 15), IR increased MSNA in the early and late phase of ischemia (70% at 5 min; 101% at 15 min). In subjects who underwent RIPC (n = 15), the increase in MSNA was delayed to the late phase of ischemia and increased only by 40%. GSH increased during ischemia in the control group (P = 0.05), but not in those who underwent RIPC. Nitrate and nitrite concentration, taken as an index of NO availability, decreased during the reperfusion period in control individuals (P < 0.05), while no change was observed in those who underwent RIPC. Experimental IR did not affect RHI in the control condition, but a significant vasodilatory response occurred in the RIPC group (P < 0.05). RIPC attenuated ischemia-induced sympathetic activation, prevented the production of an erythrocyte marker of oxidative stress and the reduction of NO availability, and ameliorated RHI.</AbstractText><CopyrightInformation>Copyright © 2016 the American Physiological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lambert</LastName><ForeName>Elisabeth A</ForeName><Initials>EA</Initials><AffiliationInfo><Affiliation>Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia; Department of Physiology, Monash University, Clayton, Victoria, Australia; and elisabeth.lambert@bakeridi.edu.au.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thomas</LastName><ForeName>Colleen J</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, Melbourne, Victoria, Australia;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hemmes</LastName><ForeName>Robyn</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eikelis</LastName><ForeName>Nina</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pathak</LastName><ForeName>Atul</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Centre de Recherche Clinique Cardiovasculaire Pasteur, Centre Hospitalier Universitaire, Toulouse, France;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schlaich</LastName><ForeName>Markus P</ForeName><Initials>MP</Initials><AffiliationInfo><Affiliation>School of Medicine and Pharmacology, Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, The University of Western Australia, Perth, Western Australia, Australia;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lambert</LastName><ForeName>Gavin W</ForeName><Initials>GW</Initials><AffiliationInfo><Affiliation>Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia; Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Victoria, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>06</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Heart Circ Physiol</MedlineTA><NlmUniqueID>100901228</NlmUniqueID><ISSNLinking>0363-6135</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>31C4KY9ESH</RegistryNumber><NameOfSubstance UI="D009569">Nitric Oxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005385" MajorTopicYN="N">Fingers</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="Y">blood supply</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005542" MajorTopicYN="N">Forearm</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D064368" MajorTopicYN="N">Healthy Volunteers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006940" MajorTopicYN="N">Hyperemia</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="Y">blood</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019194" MajorTopicYN="Y">Ischemic Preconditioning</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018482" MajorTopicYN="N">Muscle, Skeletal</DescriptorName><QualifierName UI="Q000294" MajorTopicYN="Y">innervation</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="Y">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010991" MajorTopicYN="N">Plethysmography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015427" MajorTopicYN="N">Reperfusion Injury</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="Y">blood</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013564" MajorTopicYN="N">Sympathetic Nervous System</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">endothelial function</Keyword><Keyword MajorTopicYN="N">ischemia-reperfusion injury</Keyword><Keyword MajorTopicYN="N">oxidative stress</Keyword><Keyword MajorTopicYN="N">remote conditioning</Keyword><Keyword MajorTopicYN="N">sympathetic nervous system</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>05</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>06</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>6</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>6</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>6</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27288436</ArticleId><ArticleId IdType="pii">ajpheart.00369.2016</ArticleId><ArticleId IdType="doi">10.1152/ajpheart.00369.2016</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Australie</li><li>France</li></country><region><li>Midi-Pyrénées</li><li>Occitanie (région administrative)</li></region><settlement><li>Toulouse</li></settlement></list><tree><country name="Australie"><noRegion><name sortKey="Lambert, Elisabeth A" sort="Lambert, Elisabeth A" uniqKey="Lambert E" first="Elisabeth A" last="Lambert">Elisabeth A. Lambert</name></noRegion><name sortKey="Eikelis, Nina" sort="Eikelis, Nina" uniqKey="Eikelis N" first="Nina" last="Eikelis">Nina Eikelis</name><name sortKey="Hemmes, Robyn" sort="Hemmes, Robyn" uniqKey="Hemmes R" first="Robyn" last="Hemmes">Robyn Hemmes</name><name sortKey="Lambert, Gavin W" sort="Lambert, Gavin W" uniqKey="Lambert G" first="Gavin W" last="Lambert">Gavin W. Lambert</name><name sortKey="Schlaich, Markus P" sort="Schlaich, Markus P" uniqKey="Schlaich M" first="Markus P" last="Schlaich">Markus P. Schlaich</name><name sortKey="Thomas, Colleen J" sort="Thomas, Colleen J" uniqKey="Thomas C" first="Colleen J" last="Thomas">Colleen J. Thomas</name></country><country name="France"><region name="Occitanie (région administrative)"><name sortKey="Pathak, Atul" sort="Pathak, Atul" uniqKey="Pathak A" first="Atul" last="Pathak">Atul Pathak</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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