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Article: 15-F2t-isoprostane exacerbates myocardial ischemia-reperfusion injury of isolated rat hearts

Title15-F2t-isoprostane exacerbates myocardial ischemia-reperfusion injury of isolated rat hearts
Authors
Issue Date2005
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 2005, v. 289 n. 4 58-4, p. H1366-H1372 How to Cite?
Abstract
Reactive 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.
Persistent Identifierhttp://hdl.handle.net/10722/147219
ISSN
2013 Impact Factor: 4.012
ISI Accession Number ID
References

 

Author Affiliations
  1. Hubei General Hospital
  2. University of Northern British Columbia
  3. The University of British Columbia
DC FieldValueLanguage
dc.contributor.authorXia, Zen_US
dc.contributor.authorKuo, KHen_US
dc.contributor.authorGodin, DVen_US
dc.contributor.authorWalker, MJen_US
dc.contributor.authorTao, MCYen_US
dc.contributor.authorAnsley, DMen_US
dc.date.accessioned2012-05-29T06:00:52Z-
dc.date.available2012-05-29T06:00:52Z-
dc.date.issued2005en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2005, v. 289 n. 4 58-4, p. H1366-H1372en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/147219-
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.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Pressure - Physiologyen_US
dc.subject.meshCreatine Kinase - Metabolismen_US
dc.subject.meshCreatine Kinase, Mb Formen_US
dc.subject.meshDinoprost - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshEndothelin-1 - Metabolismen_US
dc.subject.meshHeart - Drug Effects - Physiologyen_US
dc.subject.meshIsoenzymes - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardial Infarction - Metabolism - Pathology - Physiopathologyen_US
dc.subject.meshMyocardial Reperfusion Injury - Metabolism - Pathology - Physiopathologyen_US
dc.subject.meshMyocardium - Metabolism - Pathologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshVasoconstrictor Agents - Pharmacologyen_US
dc.title15-F2t-isoprostane exacerbates myocardial ischemia-reperfusion injury of isolated rat heartsen_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.doi10.1152/ajpheart.00042.2005en_US
dc.identifier.pmid15937102en_US
dc.identifier.scopuseid_2-s2.0-25444448730en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-25444448730&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume289en_US
dc.identifier.issue4 58-4en_US
dc.identifier.spageH1366en_US
dc.identifier.epageH1372en_US
dc.identifier.isiWOS:000231875300007-
dc.publisher.placeUnited Statesen_US

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