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Article: Intrathecal morphine remotely preconditions the heart via a neural pathway

TitleIntrathecal morphine remotely preconditions the heart via a neural pathway
Authors
KeywordsAnimal experiment
Apoptosis
Controlled study
Heart infarction size
Heart muscle ischemia
Issue Date2012
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal of Cardiovascular Pharmacology, 2012, v. 60 n. 2, p. 172-178 How to Cite?
AbstractCentral opioid receptor activation triggers cardioprotection against ischemia reperfusion injury, independent of peripheral opioid receptor activity. Using a rodent model of myocardial ischemia reperfusion injury with infarct size as the primary outcome, we tested the hypothesis that spinal opioids confer this beneficial effect via a neural pathway. Intrathecal morphine reduced the infarct size compared with control (23% +/- 7% vs. 58% +/- 3%, respectively, P < 0.01). Prior antagonism of the autonomic pathway, and the receptors for bradykinin, calcitonin gene-related peptide, and the KATP channel, respectively, abolished this cardioprotection (54% +/- 13%, 52% +/- 10%, 56% +/- 9%, and 49% +/- 8%, respectively, P < 0.05). In a second set of experiments, we demonstrated that the increased expression of myocardial phosphorylated-Akt and endothelial nitric oxide synthase induced by intrathecal morphine was blocked by prior administration of hexamethonium. These findings support the notion that spinal opioid receptors stimulate a neural pathway that uses nonopioid neurotransmitters to confer cardioprotection from ischemia reperfusion injury. The use of intrathecal morphine for this purpose has potential clinical application, and it is already being used in the perioperative period to provide prolonged analgesia.
Persistent Identifierhttp://hdl.handle.net/10722/159238
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWong, GTCen_US
dc.contributor.authorYao, Len_US
dc.contributor.authorXia, Zen_US
dc.contributor.authorIrwin, MGen_US
dc.date.accessioned2012-08-16T05:47:07Z-
dc.date.available2012-08-16T05:47:07Z-
dc.date.issued2012en_US
dc.identifier.citationJournal of Cardiovascular Pharmacology, 2012, v. 60 n. 2, p. 172-178en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/159238-
dc.description.abstractCentral opioid receptor activation triggers cardioprotection against ischemia reperfusion injury, independent of peripheral opioid receptor activity. Using a rodent model of myocardial ischemia reperfusion injury with infarct size as the primary outcome, we tested the hypothesis that spinal opioids confer this beneficial effect via a neural pathway. Intrathecal morphine reduced the infarct size compared with control (23% +/- 7% vs. 58% +/- 3%, respectively, P < 0.01). Prior antagonism of the autonomic pathway, and the receptors for bradykinin, calcitonin gene-related peptide, and the KATP channel, respectively, abolished this cardioprotection (54% +/- 13%, 52% +/- 10%, 56% +/- 9%, and 49% +/- 8%, respectively, P < 0.05). In a second set of experiments, we demonstrated that the increased expression of myocardial phosphorylated-Akt and endothelial nitric oxide synthase induced by intrathecal morphine was blocked by prior administration of hexamethonium. These findings support the notion that spinal opioid receptors stimulate a neural pathway that uses nonopioid neurotransmitters to confer cardioprotection from ischemia reperfusion injury. The use of intrathecal morphine for this purpose has potential clinical application, and it is already being used in the perioperative period to provide prolonged analgesia.-
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/-
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectAnimal experiment-
dc.subjectApoptosis-
dc.subjectControlled study-
dc.subjectHeart infarction size-
dc.subjectHeart muscle ischemia-
dc.titleIntrathecal morphine remotely preconditions the heart via a neural pathwayen_US
dc.typeArticleen_US
dc.identifier.emailWong, GTC: gordon@hku.hken_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.emailIrwin, MG: mgirwin@hku.hken_US
dc.identifier.authorityWong, GTC=rp00523en_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.identifier.authorityIrwin, MG=rp00390en_US
dc.description.naturepostprint-
dc.identifier.doi10.1097/FJC.0b013e31825e2195-
dc.identifier.pmid22635074-
dc.identifier.scopuseid_2-s2.0-84865602259-
dc.identifier.hkuros202218en_US
dc.identifier.volume60-
dc.identifier.issue2-
dc.identifier.spage172-
dc.identifier.epage178-
dc.identifier.isiWOS:000308006500010-
dc.publisher.placeUnited States-

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