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Article: Remote pharmacological post-conditioning by intrathecal morphine: Cardiac protection from spinal opioid receptor activation

TitleRemote pharmacological post-conditioning by intrathecal morphine: Cardiac protection from spinal 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. 9, p. 1097-1104 How to Cite?
AbstractBackground: Intrathecal morphine pre-conditioning attenuates cardiac ischemia-reperfusion injury via activation of central opioid receptors. We hypothesized that intrathecal morphine also post-conditions the myocardium in the rat. Methods: Intrathecal morphine at 0.3 μg/kg (LMPC), 3 μg/kg (MMPC) or 30 μg/kg (HMPC) was administered for 5 min before 120-min reperfusion following 30-min ischemia. Infarct size as a percentage of area at risk (IS/AAR) was determined using triphenyltetrazolium staining. MMPC was repeated following the intrathecal administration of nor BNI, NTD, CTOP, or naloxone methiodide (NM), kappa, delta, mu and non-specific opioid receptor antagonists, respectively. The role of peripheral opioid, adenosine and calcitonin gene-related peptide (CGRP) receptors was examined by the intravenous administration of NM, 8-ρ-sulfophenyl theophylline (8-SPT) and human CGRP fragment (CGRP8-37), respectively. Results: Morphine post-conditioning at all three doses was cardioprotective (IS/AAR of LMPC=37±4%, MMPC=35±5%, HMPC=32±4%, control=50±5%, P<0.01). The prior administration of opioid receptor antagonists intrathecally, as well as intravenous 8-SPT and CGRP8-37 receptor antagonists, abolished this effect (nor BNI+MMPC=47±7%, NTD+MMPC=49±7%, CTOP+MMPC=45±9%, NM+MMPC=47±6% 8-SPT+MPC=46±5% & CGRP8-37+MPC=53±6%, P=0.63). However, the intravenous administration of NM did not prevent the protective effect (34±4%, P<0.01). Conclusions: Intrathecal morphine administration can induce pharmacological cardiac post-conditioning as it involves opioid receptor centrally but non-opioid receptors peripherally. © 2010 The Acta Anaesthesiologica Scandinavica Foundation.
Persistent Identifierhttp://hdl.handle.net/10722/124464
ISSN
2015 Impact Factor: 2.049
2015 SCImago Journal Rankings: 1.020
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLing Ling, Jen_HK
dc.contributor.authorWong, GTCen_HK
dc.contributor.authorYao, Len_HK
dc.contributor.authorXia, Zen_HK
dc.contributor.authorIrwin, MGen_HK
dc.date.accessioned2010-10-31T10:35:48Z-
dc.date.available2010-10-31T10:35:48Z-
dc.date.issued2010en_HK
dc.identifier.citationActa Anaesthesiologica Scandinavica, 2010, v. 54 n. 9, p. 1097-1104en_HK
dc.identifier.issn0001-5172en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124464-
dc.description.abstractBackground: Intrathecal morphine pre-conditioning attenuates cardiac ischemia-reperfusion injury via activation of central opioid receptors. We hypothesized that intrathecal morphine also post-conditions the myocardium in the rat. Methods: Intrathecal morphine at 0.3 μg/kg (LMPC), 3 μg/kg (MMPC) or 30 μg/kg (HMPC) was administered for 5 min before 120-min reperfusion following 30-min ischemia. Infarct size as a percentage of area at risk (IS/AAR) was determined using triphenyltetrazolium staining. MMPC was repeated following the intrathecal administration of nor BNI, NTD, CTOP, or naloxone methiodide (NM), kappa, delta, mu and non-specific opioid receptor antagonists, respectively. The role of peripheral opioid, adenosine and calcitonin gene-related peptide (CGRP) receptors was examined by the intravenous administration of NM, 8-ρ-sulfophenyl theophylline (8-SPT) and human CGRP fragment (CGRP8-37), respectively. Results: Morphine post-conditioning at all three doses was cardioprotective (IS/AAR of LMPC=37±4%, MMPC=35±5%, HMPC=32±4%, control=50±5%, P<0.01). The prior administration of opioid receptor antagonists intrathecally, as well as intravenous 8-SPT and CGRP8-37 receptor antagonists, abolished this effect (nor BNI+MMPC=47±7%, NTD+MMPC=49±7%, CTOP+MMPC=45±9%, NM+MMPC=47±6% 8-SPT+MPC=46±5% & CGRP8-37+MPC=53±6%, P=0.63). However, the intravenous administration of NM did not prevent the protective effect (34±4%, P<0.01). Conclusions: Intrathecal morphine administration can induce pharmacological cardiac post-conditioning as it involves opioid receptor centrally but non-opioid receptors peripherally. © 2010 The Acta Anaesthesiologica Scandinavica Foundation.en_HK
dc.languageengen_HK
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 - administration and dosage-
dc.subject.meshIschemic Postconditioning - methods-
dc.subject.meshMorphine - administration and dosage-
dc.subject.meshMyocardial Reperfusion Injury - prevention and control-
dc.subject.meshReceptors, Opioid - drug effects - physiology-
dc.titleRemote pharmacological post-conditioning by intrathecal morphine: Cardiac protection from spinal opioid receptor activationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0001-5172&volume=54&issue=9&spage=1097&epage=1104&date=2010&atitle=Remote+pharmacological+post-conditioning+by+intrathecal+morphine:+cardiac+protection+from+spinal+opioid+receptor+activationen_HK
dc.identifier.emailWong, GTC:gordon@hku.hken_HK
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_HK
dc.identifier.emailIrwin, MG:mgirwin@hku.hken_HK
dc.identifier.authorityWong, GTC=rp00523en_HK
dc.identifier.authorityXia, Z=rp00532en_HK
dc.identifier.authorityIrwin, MG=rp00390en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1111/j.1399-6576.2010.02295.xen_HK
dc.identifier.pmid20887411-
dc.identifier.scopuseid_2-s2.0-77956416379en_HK
dc.identifier.hkuros174757en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77956416379&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume54en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1097en_HK
dc.identifier.epage1104en_HK
dc.identifier.isiWOS:000281631400008-
dc.publisher.placeDenmarken_HK
dc.identifier.citeulike7819513-

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