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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.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.publisherElsevier Science
dc.relation.ispartofjournalEuropean Journal of Pharmacology
dc.subject.fieldofresearchPharmacology and Pharmaceutical Sciences not elsewhere classified
dc.subject.fieldofresearchArtificial Intelligence and Image Processing
dc.subject.fieldofresearchCognitive Sciences
dc.subject.fieldofresearchPharmacology and Pharmaceutical Sciences
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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