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Article: Intracerebroventricular administration of morphine confers remote cardioprotection-Role of opioid receptors and calmodulin

TitleIntracerebroventricular administration of morphine confers remote cardioprotection-Role of opioid receptors and calmodulin
Authors
KeywordsHeart
Intracerebroventricular
Ischemia
Morphine
Preconditioning
Reperfusion
Issue Date2011
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 2011, v. 656 n. 1-3, p. 74-80 How to Cite?
AbstractThe current study aimed to delineate the mechanism of remote preconditioning by intracerebroventricular morphine (RMPC) against myocardial ischemia-reperfusion injury. Male Sprague-Dawley rats were given an intracerebroventricular morphine injection before myocardial ischemia and reperfusion injury. Ischemia-reperfusion injury was achieved by 30 min of left coronary artery occlusion followed by 120 min of reperfusion. The effects of remote preconditioning by intracerebroventricular morphine preconditioning were also determined upon selective blockade of the δ, κ or μ-opioid receptors, or calmodulin (CaM). The infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. Remote preconditioning by intracerebroventricular morphine reduced infarct size in the ischemic/reperfused myocardium, and the effect was abolished by the selective blockade of any one of the three δ, κ and μ opioid receptors or CaM. Furthermore, remote preconditioning by intracerebroventricular morphine increased the expression of CaM in the hippocampus and the plasma level of calcitonin gene-related peptide (CGRP). The results of the present study provide evidence that the cardioprotection of remote preconditioning by intracerebroventricular morphine involves not only all three types of opioid receptors in the central nervous system, but also CaM, which releases CGRP, one of the mediators of remote preconditioning. © 2011 Elsevier B.V.
Persistent Identifierhttp://hdl.handle.net/10722/138940
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China30672032
Excellent Youth Foundation of Anhui Scientific Committee0804106814
Funding Information:

This study was supported by grants from the National Natural Science Foundation of China (30672032) and the Excellent Youth Foundation of Anhui Scientific Committee (0804106814).

References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorIrwin, MGen_HK
dc.contributor.authorLu, Yen_HK
dc.contributor.authorMei, Ben_HK
dc.contributor.authorZuo, YMen_HK
dc.contributor.authorChen, ZWen_HK
dc.contributor.authorWong, TMen_HK
dc.date.accessioned2011-09-23T05:42:22Z-
dc.date.available2011-09-23T05:42:22Z-
dc.date.issued2011en_HK
dc.identifier.citationEuropean Journal Of Pharmacology, 2011, v. 656 n. 1-3, p. 74-80en_HK
dc.identifier.issn0014-2999en_HK
dc.identifier.urihttp://hdl.handle.net/10722/138940-
dc.description.abstractThe current study aimed to delineate the mechanism of remote preconditioning by intracerebroventricular morphine (RMPC) against myocardial ischemia-reperfusion injury. Male Sprague-Dawley rats were given an intracerebroventricular morphine injection before myocardial ischemia and reperfusion injury. Ischemia-reperfusion injury was achieved by 30 min of left coronary artery occlusion followed by 120 min of reperfusion. The effects of remote preconditioning by intracerebroventricular morphine preconditioning were also determined upon selective blockade of the δ, κ or μ-opioid receptors, or calmodulin (CaM). The infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. Remote preconditioning by intracerebroventricular morphine reduced infarct size in the ischemic/reperfused myocardium, and the effect was abolished by the selective blockade of any one of the three δ, κ and μ opioid receptors or CaM. Furthermore, remote preconditioning by intracerebroventricular morphine increased the expression of CaM in the hippocampus and the plasma level of calcitonin gene-related peptide (CGRP). The results of the present study provide evidence that the cardioprotection of remote preconditioning by intracerebroventricular morphine involves not only all three types of opioid receptors in the central nervous system, but also CaM, which releases CGRP, one of the mediators of remote preconditioning. © 2011 Elsevier B.V.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejpharen_HK
dc.relation.ispartofEuropean Journal of Pharmacologyen_HK
dc.subjectHearten_HK
dc.subjectIntracerebroventricularen_HK
dc.subjectIschemiaen_HK
dc.subjectMorphineen_HK
dc.subjectPreconditioningen_HK
dc.subjectReperfusionen_HK
dc.subject.meshCalmodulin - antagonists and inhibitors - metabolism-
dc.subject.meshCardiotonic Agents - administration and dosage - pharmacology-
dc.subject.meshCerebral Ventricles - blood supply-
dc.subject.meshMorphine - administration and dosage - pharmacology-
dc.subject.meshReceptors, Opioid - antagonists and inhibitors - metabolism-
dc.titleIntracerebroventricular administration of morphine confers remote cardioprotection-Role of opioid receptors and calmodulinen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-2999&volume=656&issue=1-3&spage=74&epage=80&date=2011&atitle=Intracerebroventricular+administration+of+morphine+confers+remote+cardioprotection:+role+of+opioid+receptors+and+calmodulin-
dc.identifier.emailIrwin, MG:mgirwin@hku.hken_HK
dc.identifier.authorityIrwin, MG=rp00390en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.ejphar.2011.01.027en_HK
dc.identifier.pmid21291882-
dc.identifier.scopuseid_2-s2.0-79952281858en_HK
dc.identifier.hkuros193683en_US
dc.identifier.hkuros216376-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79952281858&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume656en_HK
dc.identifier.issue1-3en_HK
dc.identifier.spage74en_HK
dc.identifier.epage80en_HK
dc.identifier.isiWOS:000288935600012-
dc.publisher.placeNetherlandsen_HK
dc.identifier.f1000717982082-
dc.identifier.citeulike8752256-

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