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Article: 15-F2t-isoprostane exacerbates myocardial ischemia-reperfusion injury of isolated rat hearts
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Title15-F2t-isoprostane exacerbates myocardial ischemia-reperfusion injury of isolated rat hearts
 
AuthorsXia, Z1 3
Kuo, KH2 3
Godin, DV3
Walker, MJ3
Tao, MCY3
Ansley, DM3
 
Issue Date2005
 
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
 
CitationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2005, v. 289 n. 4 58-4, p. H1366-H1372 [How to Cite?]
DOI: http://dx.doi.org/10.1152/ajpheart.00042.2005
 
AbstractReactive oxygen species induce formation of 15-F2t-isoprostane (15-F2t-IsoP), a specific marker of in vivo lipid peroxidation, which is increased after myocardial ischemia and during the subsequent reperfusion. 15-F2t-IsoP possesses potent bioactivity under pathophysiological conditions. However, it remains unknown whether 15-F2t-IsoP, by itself, can influence myocardial ischemia-reperfusion injury (IRI). Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit (KH) solution at a constant flow rate of 10 ml/min. 15-F2t-IsoP (100 nM), SQ-29548 (1 μM, SQ), a thromboxane receptor antagonist that can abolish the vasoconstrictor effect of 15-F2t-IsoP, 15-F2t-IsoP + SQ in KH, or KH alone (vehicle control) was applied for 10 rain before induction of 40 min of global ischemia followed by 60 min of reperfusion. During ischemia, saline (control), 15-F2t-IsoP, 15-F2t-IsoP + SQ, or SQ in saline was perfused through the aorta at 60 μl/min. 15-F2t-IsoP, 15-F2t-IsoP + SQ, or SQ in KH was infused during the first 15 min of reperfusion. Coronary effluent endothelin-1 concentrations were significantly higher in the group treated with 15-F2t-IsoP than in the control group during ischemia and also in the later phase of reperfusion (P < 0.05). Infusion of 15-F2t-ISoP increased release of cardiac-specific creatine kinase, reduced cardiac contractility during reperfusion, and increased myocardial infarct size relative to the control group. SQ abolished the deleterious effects of 15-F2t-IsoP. 15-F2t-IsoP exacerbates myocardial IRI and may, therefore, act as a mediator of IRI. 15-F2t-IsoP-induced endothelin-1 production during cardiac reperfusion may represent a mechanism underlying the deleterious actions of 15-F2t-IsoP. Copyright © 2005 the American Physiological Society.
 
ISSN0363-6135
2013 Impact Factor: 4.012
 
DOIhttp://dx.doi.org/10.1152/ajpheart.00042.2005
 
ISI Accession Number IDWOS:000231875300007
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorXia, Z
 
dc.contributor.authorKuo, KH
 
dc.contributor.authorGodin, DV
 
dc.contributor.authorWalker, MJ
 
dc.contributor.authorTao, MCY
 
dc.contributor.authorAnsley, DM
 
dc.date.accessioned2012-05-29T06:00:52Z
 
dc.date.available2012-05-29T06:00:52Z
 
dc.date.issued2005
 
dc.description.abstractReactive oxygen species induce formation of 15-F2t-isoprostane (15-F2t-IsoP), a specific marker of in vivo lipid peroxidation, which is increased after myocardial ischemia and during the subsequent reperfusion. 15-F2t-IsoP possesses potent bioactivity under pathophysiological conditions. However, it remains unknown whether 15-F2t-IsoP, by itself, can influence myocardial ischemia-reperfusion injury (IRI). Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit (KH) solution at a constant flow rate of 10 ml/min. 15-F2t-IsoP (100 nM), SQ-29548 (1 μM, SQ), a thromboxane receptor antagonist that can abolish the vasoconstrictor effect of 15-F2t-IsoP, 15-F2t-IsoP + SQ in KH, or KH alone (vehicle control) was applied for 10 rain before induction of 40 min of global ischemia followed by 60 min of reperfusion. During ischemia, saline (control), 15-F2t-IsoP, 15-F2t-IsoP + SQ, or SQ in saline was perfused through the aorta at 60 μl/min. 15-F2t-IsoP, 15-F2t-IsoP + SQ, or SQ in KH was infused during the first 15 min of reperfusion. Coronary effluent endothelin-1 concentrations were significantly higher in the group treated with 15-F2t-IsoP than in the control group during ischemia and also in the later phase of reperfusion (P < 0.05). Infusion of 15-F2t-ISoP increased release of cardiac-specific creatine kinase, reduced cardiac contractility during reperfusion, and increased myocardial infarct size relative to the control group. SQ abolished the deleterious effects of 15-F2t-IsoP. 15-F2t-IsoP exacerbates myocardial IRI and may, therefore, act as a mediator of IRI. 15-F2t-IsoP-induced endothelin-1 production during cardiac reperfusion may represent a mechanism underlying the deleterious actions of 15-F2t-IsoP. Copyright © 2005 the American Physiological Society.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2005, v. 289 n. 4 58-4, p. H1366-H1372 [How to Cite?]
DOI: http://dx.doi.org/10.1152/ajpheart.00042.2005
 
dc.identifier.doihttp://dx.doi.org/10.1152/ajpheart.00042.2005
 
dc.identifier.epageH1372
 
dc.identifier.isiWOS:000231875300007
 
dc.identifier.issn0363-6135
2013 Impact Factor: 4.012
 
dc.identifier.issue4 58-4
 
dc.identifier.pmid15937102
 
dc.identifier.scopuseid_2-s2.0-25444448730
 
dc.identifier.spageH1366
 
dc.identifier.urihttp://hdl.handle.net/10722/147219
 
dc.identifier.volume289
 
dc.languageeng
 
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshBlood Pressure - Physiology
 
dc.subject.meshCreatine Kinase - Metabolism
 
dc.subject.meshCreatine Kinase, Mb Form
 
dc.subject.meshDinoprost - Analogs & Derivatives - Pharmacology
 
dc.subject.meshEndothelin-1 - Metabolism
 
dc.subject.meshHeart - Drug Effects - Physiology
 
dc.subject.meshIsoenzymes - Metabolism
 
dc.subject.meshMale
 
dc.subject.meshMyocardial Infarction - Metabolism - Pathology - Physiopathology
 
dc.subject.meshMyocardial Reperfusion Injury - Metabolism - Pathology - Physiopathology
 
dc.subject.meshMyocardium - Metabolism - Pathology
 
dc.subject.meshRats
 
dc.subject.meshRats, Sprague-Dawley
 
dc.subject.meshVasoconstrictor Agents - Pharmacology
 
dc.title15-F2t-isoprostane exacerbates myocardial ischemia-reperfusion injury of isolated rat hearts
 
dc.typeArticle
 
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Author Affiliations
  1. Hubei General Hospital
  2. University of Northern British Columbia
  3. The University of British Columbia