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Article: Remifentanil preconditioning protects against ischemic injury in the intact rat heart

TitleRemifentanil preconditioning protects against ischemic injury in the intact rat heart
Authors
Issue Date2004
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.org
Citation
Anesthesiology, 2004, v. 101 n. 4, p. 918-923 How to Cite?
AbstractBackground: Opioid receptors mediate cardiac ischemic pre-conditioning. Remifentanil is a new, potent ultra-short-acting phenylpiperidlne opioid used in high doses for anesthesia. The authors hypothesize that pretreatment with this drug confers cardioprotection. Methods: Male Sprague-Dawley rats were anesthetized and the chest was opened. All animals were subjected to 30 min of occlusion of the left coronary artery and 2 h of reperfusion. Before the 30-min occlusion, rats received either preconditioning by ischemia (ischemic preconditioning, 5-min occlusion, 5-min reperfusion × 3) or pretreatment with remifentanil, performed with the same regime (3 × 5-min infusions) using 0.2, 0.6, 2, 6, or 20 μg·-kg-1·min -1 intravenously. The experiment was repeated with naltrindole (a selective δ-opioid receptor antagonist, 5 mg/kg), nor-binaltorphimine (a selective κ-OR antagonist, 5 mg/kg), or CTOP (a selective μ-opioid receptor antagonist, 1 mg/kg) administered before remifentanil-induced preconditioning or ischemic preconditioning, respectively. Infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. Results: There was a dose-related reduction in infarct size/area at risk after treatment with remifentanil that was similar to that seen with ischemic preconditioning. This effect was prevented or significantly attenuated by coadministration of a μ, κ, or δ-opioid antagonist. The infarct-sparing effect of ischemic preconditioning was abolished by blockade of κ-opioid receptors or δ-opioid receptors but not by μ-opioid receptors. Conclusion: Remifentanil mimics cardioprotection via all three opioid receptors. This differs from ischemic preconditioning, which confers cardioprotection via κ- and δ-, but not μ-opioid receptors. Part of the protective effect of remifentanil may be produced by μ-agonist activity outside the heart.
Persistent Identifierhttp://hdl.handle.net/10722/145534
ISSN
2015 Impact Factor: 5.264
2015 SCImago Journal Rankings: 2.162
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorIrwin, MGen_HK
dc.contributor.authorWong, TMen_HK
dc.date.accessioned2012-02-28T01:53:16Z-
dc.date.available2012-02-28T01:53:16Z-
dc.date.issued2004en_HK
dc.identifier.citationAnesthesiology, 2004, v. 101 n. 4, p. 918-923en_HK
dc.identifier.issn0003-3022en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145534-
dc.description.abstractBackground: Opioid receptors mediate cardiac ischemic pre-conditioning. Remifentanil is a new, potent ultra-short-acting phenylpiperidlne opioid used in high doses for anesthesia. The authors hypothesize that pretreatment with this drug confers cardioprotection. Methods: Male Sprague-Dawley rats were anesthetized and the chest was opened. All animals were subjected to 30 min of occlusion of the left coronary artery and 2 h of reperfusion. Before the 30-min occlusion, rats received either preconditioning by ischemia (ischemic preconditioning, 5-min occlusion, 5-min reperfusion × 3) or pretreatment with remifentanil, performed with the same regime (3 × 5-min infusions) using 0.2, 0.6, 2, 6, or 20 μg·-kg-1·min -1 intravenously. The experiment was repeated with naltrindole (a selective δ-opioid receptor antagonist, 5 mg/kg), nor-binaltorphimine (a selective κ-OR antagonist, 5 mg/kg), or CTOP (a selective μ-opioid receptor antagonist, 1 mg/kg) administered before remifentanil-induced preconditioning or ischemic preconditioning, respectively. Infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. Results: There was a dose-related reduction in infarct size/area at risk after treatment with remifentanil that was similar to that seen with ischemic preconditioning. This effect was prevented or significantly attenuated by coadministration of a μ, κ, or δ-opioid antagonist. The infarct-sparing effect of ischemic preconditioning was abolished by blockade of κ-opioid receptors or δ-opioid receptors but not by μ-opioid receptors. Conclusion: Remifentanil mimics cardioprotection via all three opioid receptors. This differs from ischemic preconditioning, which confers cardioprotection via κ- and δ-, but not μ-opioid receptors. Part of the protective effect of remifentanil may be produced by μ-agonist activity outside the heart.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.orgen_HK
dc.relation.ispartofAnesthesiologyen_HK
dc.subject.meshDose-Response Relationship, Drug-
dc.subject.meshIschemic Preconditioning, Myocardial-
dc.subject.meshMyocardial Ischemia - prevention and control-
dc.subject.meshMyocardial Reperfusion-
dc.subject.meshPiperidines - pharmacology-
dc.titleRemifentanil preconditioning protects against ischemic injury in the intact rat hearten_HK
dc.typeArticleen_HK
dc.identifier.emailIrwin, MG:mgirwin@hku.hken_HK
dc.identifier.authorityIrwin, MG=rp00390en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1097/00000542-200410000-00017en_HK
dc.identifier.pmid15448525-
dc.identifier.scopuseid_2-s2.0-4644325476en_HK
dc.identifier.hkuros97132en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4644325476&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume101en_HK
dc.identifier.issue4en_HK
dc.identifier.spage918en_HK
dc.identifier.epage923en_HK
dc.identifier.isiWOS:000224218400016-
dc.publisher.placeUnited Statesen_HK

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