Show simple item record

dc.contributor.authorPeart, Jasonen_US
dc.contributor.authorHeadrick, Johnen_US
dc.contributor.authorMorrison, RRen_US
dc.contributor.authorJones, Ren_US
dc.contributor.authorByford, AMen_US
dc.contributor.authorStell, AR.en_US
dc.date.accessioned2017-04-24T10:55:46Z
dc.date.available2017-04-24T10:55:46Z
dc.date.issued2000en_US
dc.identifier.issn03636135en_US
dc.identifier.urihttp://hdl.handle.net/10072/3465
dc.description.abstractThe role of A1adenosine receptors (A1AR) in ischemic preconditioning was investigated in isolated crystalloid-perfused wild-type and transgenic mouse hearts with increased A1AR. The effect of preconditioning on postischemic myocardial function, lactate dehydrogenase (LDH) release, and infarct size was examined. Functional recovery was greater in transgenic versus wild-type hearts (44.8 ᠳ.4% baseline vs. 25.6 ᠱ.7%). Preconditioning improved functional recovery in wild-type hearts from 25.6 ᠱ.7% to 37.4 ᠲ.2% but did not change recovery in transgenic hearts (44.8 ᠳ.4% vs. 44.5 ᠳ.9%). In isovolumically contracting hearts, pretreatment with selective A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine attenuated the improved functional recovery in both wild-type preconditioned (74.2 ᠷ.3% baseline rate of pressure development over time untreated vs. 29.7 ᠷ.3% treated) and transgenic hearts (84.1 ᠱ2.8% untreated vs. 42.1 ᠶ.8% treated). Preconditioning wild-type hearts reduced LDH release (from 7,012 ᠱ,451 to 1,691 ᠱ,256 U 砬-1 砧-1 砭in-1) and infarct size (from 62.6 ᠵ.1% to 32.3 ᠱ1.5%). Preconditioning did not affect LDH release or infarct size in hearts overexpressing A1AR. Compared with wild-type hearts, A1AR overexpression markedly reduced LDH release (from 7,012 ᠱ,451 to 917 ᠱ,123 U 砬-1 砧-1 砭in-1) and infarct size (from 62.6 ᠵ.1% to 6.5 ᠲ.1%). These data demonstrate that murine preconditioning involves endogenous activation of A1AR. The beneficial effects of preconditioning and A1AR overexpression are not additive. Taken with the observation that A1AR blockade equally eliminates the functional protection resulting from both preconditioning and transgenic A1AR overexpression, we conclude that the two interventions affect cardioprotection via common mechanisms or pathways.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_US
dc.languageEnglishen_US
dc.language.isoen_US
dc.publisherAmerican Physiological Societyen_US
dc.publisher.placeUSAen_US
dc.publisher.urihttp://ajpheart.physiology.org/content/279/3/H1071en_US
dc.relation.ispartofpagefromH1071en_US
dc.relation.ispartofpagetoH1078en_US
dc.relation.ispartofjournalAmerican Journal of Physiology: Heart and Circulatory Physiologyen_US
dc.relation.ispartofvolume279en_US
dc.subject.fieldofresearchcode320000en_US
dc.titleTransgenic overexpression of cardiac A1 adenosine receptors mimics ischemic preconditioningen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.facultyGriffith Health, School of Medical Scienceen_US
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.en_US
gro.date.issued2015-02-05T03:42:08Z
gro.hasfulltextNo Full Text


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record