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Article: Activation of central opioid receptors induces cardioprotection against ischemia-reperfusion injury

TitleActivation of central opioid receptors induces cardioprotection against ischemia-reperfusion injury
Authors
Issue Date2010
PublisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.org
Citation
Anesthesia And Analgesia, 2010, v. 111 n. 1, p. 24-28 How to Cite?
AbstractBACKGROUND: Small doses of intrathecal morphine provide cardioprotection similar to that conferred by IV morphine and ischemic preconditioning (IPC). We investigated the relative role of central versus peripheral opioid receptors in intrathecal morphine preconditioning (ITMPC). METHODS: Forty-eight anesthetized, open-chest, male Sprague-Dawley rats were assigned to 1 of 7 treatment groups (n = 6-7) after successful intrathecal catheter placement. ITMPC was achieved by 3 consecutive 5-min intrathecal infusions of morphine (1.0 μ-g/kg each). This was repeated in the presence of either IV (IV naloxone methiodide + ITMPC) or intrathecally (intrathecal naloxone methiodide [ITNM] + ITMPC) administered naloxone methiodide. This compound was also given via these same routes in the absence of ITMPC (IV naloxone methiodide + ITNM). Intrathecal normal saline and IPC were used as negative and positive controls, respectively. Myocardial ischemia and reperfusion injury were induced by 30 min of left main coronary artery occlusion followed by 2 h of reperfusion. Myocardial infarct size, as a percentage of the area-at-risk, was determined by 2,3,5-triphenyltetrazolium staining. RESULTS: The infarct size/area-at-risk were significantly reduced in the IPC (22% ± 3%) and ITMPC (26% ± 5%) groups compared with the control group (48% ± 9%) (P< 0.01). The addition of ITNM reversed the cardioprotective effects of ITMPC (45% ± 4%), whereas IV administration of the drug did not have any effect on ITMPC (28% ± 9%, P < 0.01). CONCLUSIONS: Intrathecally administered morphine can produce cardioprotective effects via the activation of central opioid receptors, without the apparent involvement of peripheral opioid receptors. Copyright © 2010 International Anesthesia Research Society.
Persistent Identifierhttp://hdl.handle.net/10722/147276
ISSN
2015 Impact Factor: 3.827
2015 SCImago Journal Rankings: 1.523
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, GTCen_US
dc.contributor.authorLing, JLen_US
dc.contributor.authorIrwin, MGen_US
dc.date.accessioned2012-05-29T06:01:10Z-
dc.date.available2012-05-29T06:01:10Z-
dc.date.issued2010en_US
dc.identifier.citationAnesthesia And Analgesia, 2010, v. 111 n. 1, p. 24-28en_US
dc.identifier.issn0003-2999en_US
dc.identifier.urihttp://hdl.handle.net/10722/147276-
dc.description.abstractBACKGROUND: Small doses of intrathecal morphine provide cardioprotection similar to that conferred by IV morphine and ischemic preconditioning (IPC). We investigated the relative role of central versus peripheral opioid receptors in intrathecal morphine preconditioning (ITMPC). METHODS: Forty-eight anesthetized, open-chest, male Sprague-Dawley rats were assigned to 1 of 7 treatment groups (n = 6-7) after successful intrathecal catheter placement. ITMPC was achieved by 3 consecutive 5-min intrathecal infusions of morphine (1.0 μ-g/kg each). This was repeated in the presence of either IV (IV naloxone methiodide + ITMPC) or intrathecally (intrathecal naloxone methiodide [ITNM] + ITMPC) administered naloxone methiodide. This compound was also given via these same routes in the absence of ITMPC (IV naloxone methiodide + ITNM). Intrathecal normal saline and IPC were used as negative and positive controls, respectively. Myocardial ischemia and reperfusion injury were induced by 30 min of left main coronary artery occlusion followed by 2 h of reperfusion. Myocardial infarct size, as a percentage of the area-at-risk, was determined by 2,3,5-triphenyltetrazolium staining. RESULTS: The infarct size/area-at-risk were significantly reduced in the IPC (22% ± 3%) and ITMPC (26% ± 5%) groups compared with the control group (48% ± 9%) (P< 0.01). The addition of ITNM reversed the cardioprotective effects of ITMPC (45% ± 4%), whereas IV administration of the drug did not have any effect on ITMPC (28% ± 9%, P < 0.01). CONCLUSIONS: Intrathecally administered morphine can produce cardioprotective effects via the activation of central opioid receptors, without the apparent involvement of peripheral opioid receptors. Copyright © 2010 International Anesthesia Research Society.en_US
dc.languageengen_US
dc.publisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.orgen_US
dc.relation.ispartofAnesthesia and Analgesiaen_US
dc.subject.meshAnalgesics, Opioid - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Pressure - Drug Effectsen_US
dc.subject.meshCardiotonic Agents - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Physiologyen_US
dc.subject.meshHeart Rate - Drug Effectsen_US
dc.subject.meshInjections, Spinalen_US
dc.subject.meshIschemic Preconditioning, Myocardial - Methodsen_US
dc.subject.meshMaleen_US
dc.subject.meshMorphine - Pharmacologyen_US
dc.subject.meshMyocardial Infarction - Pathologyen_US
dc.subject.meshMyocardial Reperfusion Injury - Prevention & Controlen_US
dc.subject.meshMyocardium - Pathologyen_US
dc.subject.meshNaloxone - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshNarcotic Antagonists - Pharmacologyen_US
dc.subject.meshQuaternary Ammonium Compounds - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Opioid - Agonistsen_US
dc.titleActivation of central opioid receptors induces cardioprotection against ischemia-reperfusion injuryen_US
dc.typeArticleen_US
dc.identifier.emailWong, GTC:gordon@hku.hken_US
dc.identifier.emailIrwin, MG:mgirwin@hku.hken_US
dc.identifier.authorityWong, GTC=rp00523en_US
dc.identifier.authorityIrwin, MG=rp00390en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1213/ANE.0b013e3181b8b77een_US
dc.identifier.pmid19861363-
dc.identifier.scopuseid_2-s2.0-77954680385en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77954680385&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume111en_US
dc.identifier.issue1en_US
dc.identifier.spage24en_US
dc.identifier.epage28en_US
dc.identifier.eissn1526-7598-
dc.identifier.isiWOS:000279281500009-
dc.publisher.placeUnited Statesen_US
dc.identifier.f10004277956-

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