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Article: Endothelin A and B receptor antagonist bosentan reduces postischemic myocardial injury in the rat: Critical timing of administration

TitleEndothelin A and B receptor antagonist bosentan reduces postischemic myocardial injury in the rat: Critical timing of administration
Authors
Issue Date2005
PublisherN R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjpp
Citation
Canadian Journal Of Physiology And Pharmacology, 2005, v. 83 n. 3, p. 259-266 How to Cite?
AbstractThe purpose of this study was to investigate the effects of bosentan, a mixed endothelin receptor A and B subtype antagonist, on myocardial ischemia-reperfusion injury and to explore the influence of the timing of bosentan administration on its cardioprotective effects. Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit solution (KH) at a constant flow rate at 10 mL/min. Global myocardial ischemia was induced by stopping KH perfusion for 40 min, and this was followed by 60 min of reperfusion. Hearts were randomized to 1 of 3 experimental groups (n = 1 each): untreated control; treatment with bosentan 1 μmol/L 10 min prior to, during 40 min global ischemia, and for 15 min of reperfusion (BOS); or treatment with bosentan 1 μmol/L after 15 min of reperfusion (BOS-R). We observed that BOS-R, but not the BOS treatment regimen, significantly reduced the release of cardiac-specific creatine kinase and postischemic myocardial infarct size (P < 0.05 vs. control) without affecting myocardial contractility. Left ventricular developed pressure in the BOS group was significantly (P < 0.01) lower than that in the control group throughout reperfusion. It is concluded that pharmacologically delayed antagonism of endothelin-1 during reperfusion attenuates postischemic myocardial injury. Endothelin-1 antagonist application during early reperfusion may exacerbate postischemic myocardial dysfunction. © 2005 NRC Canada.
Persistent Identifierhttp://hdl.handle.net/10722/147214
ISSN
2014 Impact Factor: 1.770
2014 SCImago Journal Rankings: 0.611
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXia, Zen_US
dc.contributor.authorKuo, KHen_US
dc.contributor.authorMcneill, JHen_US
dc.contributor.authorAnsley, DMen_US
dc.date.accessioned2012-05-29T06:00:50Z-
dc.date.available2012-05-29T06:00:50Z-
dc.date.issued2005en_US
dc.identifier.citationCanadian Journal Of Physiology And Pharmacology, 2005, v. 83 n. 3, p. 259-266en_US
dc.identifier.issn0008-4212en_US
dc.identifier.urihttp://hdl.handle.net/10722/147214-
dc.description.abstractThe purpose of this study was to investigate the effects of bosentan, a mixed endothelin receptor A and B subtype antagonist, on myocardial ischemia-reperfusion injury and to explore the influence of the timing of bosentan administration on its cardioprotective effects. Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit solution (KH) at a constant flow rate at 10 mL/min. Global myocardial ischemia was induced by stopping KH perfusion for 40 min, and this was followed by 60 min of reperfusion. Hearts were randomized to 1 of 3 experimental groups (n = 1 each): untreated control; treatment with bosentan 1 μmol/L 10 min prior to, during 40 min global ischemia, and for 15 min of reperfusion (BOS); or treatment with bosentan 1 μmol/L after 15 min of reperfusion (BOS-R). We observed that BOS-R, but not the BOS treatment regimen, significantly reduced the release of cardiac-specific creatine kinase and postischemic myocardial infarct size (P < 0.05 vs. control) without affecting myocardial contractility. Left ventricular developed pressure in the BOS group was significantly (P < 0.01) lower than that in the control group throughout reperfusion. It is concluded that pharmacologically delayed antagonism of endothelin-1 during reperfusion attenuates postischemic myocardial injury. Endothelin-1 antagonist application during early reperfusion may exacerbate postischemic myocardial dysfunction. © 2005 NRC Canada.en_US
dc.languageengen_US
dc.publisherN R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjppen_US
dc.relation.ispartofCanadian Journal of Physiology and Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCreatine Kinase - Metabolismen_US
dc.subject.meshCreatine Kinase, Mb Formen_US
dc.subject.meshDrug Administration Scheduleen_US
dc.subject.meshEndothelin-1 - Metabolismen_US
dc.subject.meshHeart - Drug Effectsen_US
dc.subject.meshIsoenzymes - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardial Contraction - Drug Effectsen_US
dc.subject.meshMyocardial Ischemia - Metabolismen_US
dc.subject.meshMyocardial Reperfusion Injury - Metabolism - Prevention & Controlen_US
dc.subject.meshMyocardium - Metabolism - Pathologyen_US
dc.subject.meshRatsen_US
dc.subject.meshReceptor, Endothelin A - Antagonists & Inhibitorsen_US
dc.subject.meshReceptor, Endothelin B - Antagonists & Inhibitorsen_US
dc.subject.meshSulfonamides - Administration & Dosage - Pharmacologyen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshVentricular Pressure - Drug Effectsen_US
dc.titleEndothelin A and B receptor antagonist bosentan reduces postischemic myocardial injury in the rat: Critical timing of administrationen_US
dc.typeArticleen_US
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1139/y05-014en_US
dc.identifier.pmid15870840-
dc.identifier.scopuseid_2-s2.0-21744453970en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-21744453970&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume83en_US
dc.identifier.issue3en_US
dc.identifier.spage259en_US
dc.identifier.epage266en_US
dc.identifier.isiWOS:000229413700004-
dc.publisher.placeCanadaen_US

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