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Article: Remifentanil post-conditioning attenuates cardiac ischemia-reperfusion injury via κ or δ opioid receptor activation

TitleRemifentanil post-conditioning attenuates cardiac ischemia-reperfusion injury via κ or δ opioid receptor activation
Authors
Issue Date2010
PublisherBlackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journals/AAS
Citation
Acta Anaesthesiologica Scandinavica, 2010, v. 54 n. 4, p. 510-518 How to Cite?
AbstractBackground: Ischemic pre- or post-conditioning of the heart has been shown to involve opioid receptors. Remifentanil, an ultra-short-acting selective μ opioid receptor agonist in clinical use, pre-conditions the rat heart against ischemia-reperfusion injury. This study investigates whether remifentanil post-conditioning is also cardioprotective. Methods: Remifentanil post-conditioning (5-min infusion at 1, 5, 10 or 20 μg/kg/min) or ischemic post-conditioning (three cycles of a 10 s reperfusion interspersed with a 10 s ischemia) was induced in an open-chest rat heart model of ischemia and reperfusion injury, in the presence or absence of nor-binaltorphimine, naltrindole or CTOP, specific κ, δ and μ opioid receptor antagonists, respectively. The same sequence of experiments was repeated in the isolated heart model using the maximal protective dose of remifentanil from the dose-response studies. Results: Both ischemic and remifentanil post-conditioning reduced the myocardial infarct size relative to the control group in both models. This cardioprotective effect for both post-conditioning regimes was prevented by the prior administration of nor-binaltorphimine and naltrindole but not CTOP. The sole administration of the antagonists had no effect on the size of myocardial infarction. Conclusions: These results indicate that remifentanil post-conditioning protects the heart from ischemia-reperfusion injury to a similar extent as of ischemic post-conditioning. This protection involves κ and δ but not μ opioid receptor activation. This drug has great potential as a clinical post-conditioning modality as it can be given in large doses without prolonged opioid-related side effects. © 2009 The Acta Anaesthesiologica Scandinavica Foundation.
Persistent Identifierhttp://hdl.handle.net/10722/60990
ISSN
2015 Impact Factor: 2.049
2015 SCImago Journal Rankings: 1.020
ISI Accession Number ID
Funding AgencyGrant Number
Department of Anaesthesiology, University of Hong Kong
University of Hong Kong
Funding Information:

This work was performed in the Department of Anaesthesiology, University of Hong Kong, and was funded in part by the Small Project Fund, University of Hong Kong. It has been presented in part at the Annual Scientific Meeting of the Australian and New Zealand College of Anaesthetists in Sydney, Australia, on 6 May 2008.

References

 

DC FieldValueLanguage
dc.contributor.authorWong, GTCen_HK
dc.contributor.authorLi, Ren_HK
dc.contributor.authorJiang, LLen_HK
dc.contributor.authorIrwin, MGen_HK
dc.date.accessioned2010-06-03T04:23:02Z-
dc.date.available2010-06-03T04:23:02Z-
dc.date.issued2010en_HK
dc.identifier.citationActa Anaesthesiologica Scandinavica, 2010, v. 54 n. 4, p. 510-518en_HK
dc.identifier.issn0001-5172en_HK
dc.identifier.urihttp://hdl.handle.net/10722/60990-
dc.description.abstractBackground: Ischemic pre- or post-conditioning of the heart has been shown to involve opioid receptors. Remifentanil, an ultra-short-acting selective μ opioid receptor agonist in clinical use, pre-conditions the rat heart against ischemia-reperfusion injury. This study investigates whether remifentanil post-conditioning is also cardioprotective. Methods: Remifentanil post-conditioning (5-min infusion at 1, 5, 10 or 20 μg/kg/min) or ischemic post-conditioning (three cycles of a 10 s reperfusion interspersed with a 10 s ischemia) was induced in an open-chest rat heart model of ischemia and reperfusion injury, in the presence or absence of nor-binaltorphimine, naltrindole or CTOP, specific κ, δ and μ opioid receptor antagonists, respectively. The same sequence of experiments was repeated in the isolated heart model using the maximal protective dose of remifentanil from the dose-response studies. Results: Both ischemic and remifentanil post-conditioning reduced the myocardial infarct size relative to the control group in both models. This cardioprotective effect for both post-conditioning regimes was prevented by the prior administration of nor-binaltorphimine and naltrindole but not CTOP. The sole administration of the antagonists had no effect on the size of myocardial infarction. Conclusions: These results indicate that remifentanil post-conditioning protects the heart from ischemia-reperfusion injury to a similar extent as of ischemic post-conditioning. This protection involves κ and δ but not μ opioid receptor activation. This drug has great potential as a clinical post-conditioning modality as it can be given in large doses without prolonged opioid-related side effects. © 2009 The Acta Anaesthesiologica Scandinavica Foundation.en_HK
dc.languageeng-
dc.publisherBlackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journals/AASen_HK
dc.relation.ispartofActa Anaesthesiologica Scandinavicaen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.subject.meshAnalgesics, Opioid - pharmacology-
dc.subject.meshCardiotonic Agents-
dc.subject.meshMyocardial Reperfusion Injury - drug therapy - pathology-
dc.subject.meshReceptors, Opioid, delta - agonists - antagonists and inhibitors-
dc.subject.meshReceptors, Opioid, kappa - agonists - antagonists and inhibitors-
dc.titleRemifentanil post-conditioning attenuates cardiac ischemia-reperfusion injury via κ or δ opioid receptor activationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0001-5172&volume=54&issue=4&spage=510&epage=518&date=2010&atitle=Remifentanil+post-conditioning+attenuates+cardiac+Ischemia-reperfusion+injury+via+κ+or+δ+opioid++receptor+activation-
dc.identifier.emailWong, GTC:gordon@hku.hken_HK
dc.identifier.emailIrwin, MG:mgirwin@hku.hken_HK
dc.identifier.authorityWong, GTC=rp00523en_HK
dc.identifier.authorityIrwin, MG=rp00390en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1111/j.1399-6576.2009.02145.xen_HK
dc.identifier.pmid19878098-
dc.identifier.scopuseid_2-s2.0-77649214410en_HK
dc.identifier.hkuros169783-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77649214410&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume54en_HK
dc.identifier.issue4en_HK
dc.identifier.spage510en_HK
dc.identifier.epage518en_HK
dc.identifier.eissn1399-6576-
dc.identifier.isiWOS:000274932800019-
dc.publisher.placeDenmarken_HK
dc.identifier.citeulike6822842-

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