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Article: Remote pharmacological post-conditioning by intrathecal morphine: Cardiac protection from spinal opioid receptor activation
Title | Remote pharmacological post-conditioning by intrathecal morphine: Cardiac protection from spinal opioid receptor activation |
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Authors | |
Issue Date | 2010 |
Publisher | Blackwell 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? |
Abstract | Background: 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 Identifier | http://hdl.handle.net/10722/124464 |
ISSN | 2023 Impact Factor: 1.9 2023 SCImago Journal Rankings: 0.743 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Ling Ling, J | en_HK |
dc.contributor.author | Wong, GTC | en_HK |
dc.contributor.author | Yao, L | en_HK |
dc.contributor.author | Xia, Z | en_HK |
dc.contributor.author | Irwin, MG | en_HK |
dc.date.accessioned | 2010-10-31T10:35:48Z | - |
dc.date.available | 2010-10-31T10:35:48Z | - |
dc.date.issued | 2010 | en_HK |
dc.identifier.citation | Acta Anaesthesiologica Scandinavica, 2010, v. 54 n. 9, p. 1097-1104 | en_HK |
dc.identifier.issn | 0001-5172 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/124464 | - |
dc.description.abstract | Background: 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.language | eng | en_HK |
dc.publisher | Blackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journals/AAS | en_HK |
dc.relation.ispartof | Acta Anaesthesiologica Scandinavica | en_HK |
dc.rights | The definitive version is available at www.blackwell-synergy.com | - |
dc.subject.mesh | Analgesics, Opioid - administration and dosage | - |
dc.subject.mesh | Ischemic Postconditioning - methods | - |
dc.subject.mesh | Morphine - administration and dosage | - |
dc.subject.mesh | Myocardial Reperfusion Injury - prevention and control | - |
dc.subject.mesh | Receptors, Opioid - drug effects - physiology | - |
dc.title | Remote pharmacological post-conditioning by intrathecal morphine: Cardiac protection from spinal opioid receptor activation | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+activation | en_HK |
dc.identifier.email | Wong, GTC:gordon@hku.hk | en_HK |
dc.identifier.email | Xia, Z:zyxia@hkucc.hku.hk | en_HK |
dc.identifier.email | Irwin, MG:mgirwin@hku.hk | en_HK |
dc.identifier.authority | Wong, GTC=rp00523 | en_HK |
dc.identifier.authority | Xia, Z=rp00532 | en_HK |
dc.identifier.authority | Irwin, MG=rp00390 | en_HK |
dc.description.nature | postprint | - |
dc.identifier.doi | 10.1111/j.1399-6576.2010.02295.x | en_HK |
dc.identifier.pmid | 20887411 | - |
dc.identifier.scopus | eid_2-s2.0-77956416379 | en_HK |
dc.identifier.hkuros | 174757 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-77956416379&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 54 | en_HK |
dc.identifier.issue | 9 | en_HK |
dc.identifier.spage | 1097 | en_HK |
dc.identifier.epage | 1104 | en_HK |
dc.identifier.isi | WOS:000281631400008 | - |
dc.publisher.place | Denmark | en_HK |
dc.identifier.citeulike | 7819513 | - |
dc.identifier.issnl | 0001-5172 | - |