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Article: Endothelin A and B receptor antagonist bosentan reduces postischemic myocardial injury in the rat: Critical timing of administration
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TitleEndothelin A and B receptor antagonist bosentan reduces postischemic myocardial injury in the rat: Critical timing of administration
 
AuthorsXia, Z1
Kuo, KH1
Mcneill, JH1
Ansley, DM1
 
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
 
CitationCanadian Journal Of Physiology And Pharmacology, 2005, v. 83 n. 3, p. 259-266 [How to Cite?]
DOI: http://dx.doi.org/10.1139/y05-014
 
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.
 
ISSN0008-4212
2013 Impact Factor: 1.546
 
DOIhttp://dx.doi.org/10.1139/y05-014
 
ISI Accession Number IDWOS:000229413700004
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorXia, Z
 
dc.contributor.authorKuo, KH
 
dc.contributor.authorMcneill, JH
 
dc.contributor.authorAnsley, DM
 
dc.date.accessioned2012-05-29T06:00:50Z
 
dc.date.available2012-05-29T06:00:50Z
 
dc.date.issued2005
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationCanadian Journal Of Physiology And Pharmacology, 2005, v. 83 n. 3, p. 259-266 [How to Cite?]
DOI: http://dx.doi.org/10.1139/y05-014
 
dc.identifier.doihttp://dx.doi.org/10.1139/y05-014
 
dc.identifier.epage266
 
dc.identifier.isiWOS:000229413700004
 
dc.identifier.issn0008-4212
2013 Impact Factor: 1.546
 
dc.identifier.issue3
 
dc.identifier.pmid15870840
 
dc.identifier.scopuseid_2-s2.0-21744453970
 
dc.identifier.spage259
 
dc.identifier.urihttp://hdl.handle.net/10722/147214
 
dc.identifier.volume83
 
dc.languageeng
 
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?cjpp
 
dc.publisher.placeCanada
 
dc.relation.ispartofCanadian Journal of Physiology and Pharmacology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshCreatine Kinase - Metabolism
 
dc.subject.meshCreatine Kinase, Mb Form
 
dc.subject.meshDrug Administration Schedule
 
dc.subject.meshEndothelin-1 - Metabolism
 
dc.subject.meshHeart - Drug Effects
 
dc.subject.meshIsoenzymes - Metabolism
 
dc.subject.meshMale
 
dc.subject.meshMyocardial Contraction - Drug Effects
 
dc.subject.meshMyocardial Ischemia - Metabolism
 
dc.subject.meshMyocardial Reperfusion Injury - Metabolism - Prevention & Control
 
dc.subject.meshMyocardium - Metabolism - Pathology
 
dc.subject.meshRats
 
dc.subject.meshReceptor, Endothelin A - Antagonists & Inhibitors
 
dc.subject.meshReceptor, Endothelin B - Antagonists & Inhibitors
 
dc.subject.meshSulfonamides - Administration & Dosage - Pharmacology
 
dc.subject.meshTime Factors
 
dc.subject.meshVentricular Pressure - Drug Effects
 
dc.titleEndothelin A and B receptor antagonist bosentan reduces postischemic myocardial injury in the rat: Critical timing of administration
 
dc.typeArticle
 
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<description.abstract>The 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 &#956;mol/L 10 min prior to, during 40 min global ischemia, and for 15 min of reperfusion (BOS); or treatment with bosentan 1 &#956;mol/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 &lt; 0.05 vs. control) without affecting myocardial contractility. Left ventricular developed pressure in the BOS group was significantly (P &lt; 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. &#169; 2005 NRC Canada.</description.abstract>
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Author Affiliations
  1. The University of British Columbia