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dc.contributor.authorHoe, Louise E See
dc.contributor.authorSchilling, Jan M
dc.contributor.authorBusija, Anna R
dc.contributor.authorHaushalter, Kristofer J
dc.contributor.authorOzberk, Victoria
dc.contributor.authorKeshwani, Malik M
dc.contributor.authorRoth, David M
dc.contributor.authorDu Toit, Eugene
dc.contributor.authorHeadrick, John P
dc.contributor.authorPatel, Hemal H
dc.contributor.authorPeart, Jason N
dc.date.accessioned2018-01-23T01:27:14Z
dc.date.available2018-01-23T01:27:14Z
dc.date.issued2016
dc.identifier.issn0014-2999
dc.identifier.doi10.1016/j.ejphar.2016.06.054
dc.identifier.urihttp://hdl.handle.net/10072/100466
dc.description.abstractβ-adrenoceptor antagonists are commonly used in ischaemic heart disease (IHD) patients, yet may impair signalling and efficacy of ‘cardioprotective’ interventions. We assessed effects of chronic β1-adrenoceptor antagonism on myocardial resistance to ischaemia-reperfusion (IR) injury and the ability of cardioprotective interventions [classic ischaemic preconditioning (IPC); novel sustained ligand-activated preconditioning (SLP)] to reduce IR injury in murine hearts. Young male C57Bl/6 mice were untreated or received atenolol (0.5 g/l in drinking water) for 4 weeks. Subsequently, two cardioprotective stimuli were evaluated: morphine pellets implanted (to induce SLP, controls received placebo) 5 days prior to Langendorff heart perfusion, and IPC in perfused hearts (3×1.5 min ischaemia/2 min reperfusion). Atenolol significantly reduced in vivo heart rate. Untreated control hearts exhibited substantial left ventricular dysfunction (~50% pressure development recovery, ~20 mmHg diastolic pressure rise) with significant release of lactate dehydrogenase (LDH, tissue injury indicator) after 25 min ischaemia/45 min reperfusion. Contractile dysfunction and elevated LDH were reduced >50% with IPC and SLP. While atenolol treatment did not modify baseline contractile function, post-ischaemic function was significantly depressed compared to untreated hearts. Atenolol pre-treatment abolished beneficial effects of IPC, whereas SLP protection was preserved. These data indicate that chronic β1-adrenoceptor blockade can exert negative effects on functional IR tolerance and negate conventional IPC (implicating β1-adrenoceptors in IR injury and IPC signalling). However, novel morphine-induced SLP is resistant to inhibition by β1-adrenoceptor antagonism.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherElsevier Science
dc.relation.ispartofpagefrom1
dc.relation.ispartofpageto7
dc.relation.ispartofjournalEuropean Journal of Pharmacology
dc.relation.ispartofvolume789
dc.subject.fieldofresearchPharmacology and Pharmaceutical Sciences not elsewhere classified
dc.subject.fieldofresearchArtificial Intelligence and Image Processing
dc.subject.fieldofresearchPsychology
dc.subject.fieldofresearchCognitive Sciences
dc.subject.fieldofresearchPharmacology and Pharmaceutical Sciences
dc.subject.fieldofresearchcode111599
dc.subject.fieldofresearchcode0801
dc.subject.fieldofresearchcode1701
dc.subject.fieldofresearchcode1702
dc.subject.fieldofresearchcode1115
dc.titleChronic β1-adrenoceptor blockade impairs ischaemic tolerance and preconditioning in murine myocardium
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.facultyGriffith Health, School of Medical Science
gro.hasfulltextNo Full Text
gro.griffith.authorHeadrick, John P.
gro.griffith.authorPeart, Jason N.
gro.griffith.authorSee Hoe, Louise
gro.griffith.authorDu Toit, Eugene
gro.griffith.authorOzberk, Victoria


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