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Article: Propofol enhances ischemic tolerance of middle-aged rat hearts: Effects on 15-F2t-isoprostane formation and tissue antioxidant capacity

TitlePropofol enhances ischemic tolerance of middle-aged rat hearts: Effects on 15-F2t-isoprostane formation and tissue antioxidant capacity
Authors
Issue Date2003
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 2003, v. 59 n. 1, p. 113-121 How to Cite?
Abstract
Objective: Experimental study has shown that myocardial ischemic tolerance is reduced during middle-age. We investigated the effect of propofol on ischemic tolerance of middle-aged rat hearts. Methods: Hearts of young adult (10 weeks old, Y) and middle-aged rats (20 weeks old, M) were assigned to propofol (P-Y, P-M) and control (C-Y, C-M) groups (n=6 each). Hearts were perfused using a Langendorff preparation with Krebs-Henseleit solution (KH) at constant flow rates. We applied propofol (P-Y, P-M) for 10 min at 12 μg/ml before inducing 40 min global ischemia. During ischemia, saline (C-Y, C-M) or propofol (P-Y, P-M) in saline was perfused through the aorta at 60 μl/min. Propofol in KH was perfused at 12 μg/ml for the first 15 min of reperfusion and subsequently reduced to 5 μg/ml in propofol treatment groups. Coronary effluent was assayed for 15-F2t-isoprostane after equilibration, during ischemia (T1) and at 0.5 (T2) and 5 (T3) min of reperfusion. After 90 min of reperfusion (T4), hearts were harvested to assess tissue antioxidant capacity. Results: In P-Y, we observed an increased latency to ischemic-contracture and a significantly reduced contracture after 35 min ischemia compared to control groups. No ischemic contracture was observed in P-M. There were significantly lower 15-F2t-isoprostane levels in P-M and P-Y than in C-M and C-Y at T1. At T4, the recovery of left ventricular developed pressure in P-M was greater than in P-Y (P<0.05); both were greater than in C-M and C-Y. Conclusion: Propofol enhanced ischemic tolerance of middle-aged hearts, primarily by inhibiting lipid peroxidation. © 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/147202
ISSN
2013 Impact Factor: 5.808
2013 SCImago Journal Rankings: 2.799
ISI Accession Number ID
References

 

Author Affiliations
  1. The University of British Columbia
DC FieldValueLanguage
dc.contributor.authorXia, Zen_US
dc.contributor.authorGodin, DVen_US
dc.contributor.authorAnsley, DMen_US
dc.date.accessioned2012-05-29T06:00:45Z-
dc.date.available2012-05-29T06:00:45Z-
dc.date.issued2003en_US
dc.identifier.citationCardiovascular Research, 2003, v. 59 n. 1, p. 113-121en_US
dc.identifier.issn0008-6363en_US
dc.identifier.urihttp://hdl.handle.net/10722/147202-
dc.description.abstractObjective: Experimental study has shown that myocardial ischemic tolerance is reduced during middle-age. We investigated the effect of propofol on ischemic tolerance of middle-aged rat hearts. Methods: Hearts of young adult (10 weeks old, Y) and middle-aged rats (20 weeks old, M) were assigned to propofol (P-Y, P-M) and control (C-Y, C-M) groups (n=6 each). Hearts were perfused using a Langendorff preparation with Krebs-Henseleit solution (KH) at constant flow rates. We applied propofol (P-Y, P-M) for 10 min at 12 μg/ml before inducing 40 min global ischemia. During ischemia, saline (C-Y, C-M) or propofol (P-Y, P-M) in saline was perfused through the aorta at 60 μl/min. Propofol in KH was perfused at 12 μg/ml for the first 15 min of reperfusion and subsequently reduced to 5 μg/ml in propofol treatment groups. Coronary effluent was assayed for 15-F2t-isoprostane after equilibration, during ischemia (T1) and at 0.5 (T2) and 5 (T3) min of reperfusion. After 90 min of reperfusion (T4), hearts were harvested to assess tissue antioxidant capacity. Results: In P-Y, we observed an increased latency to ischemic-contracture and a significantly reduced contracture after 35 min ischemia compared to control groups. No ischemic contracture was observed in P-M. There were significantly lower 15-F2t-isoprostane levels in P-M and P-Y than in C-M and C-Y at T1. At T4, the recovery of left ventricular developed pressure in P-M was greater than in P-Y (P<0.05); both were greater than in C-M and C-Y. Conclusion: Propofol enhanced ischemic tolerance of middle-aged hearts, primarily by inhibiting lipid peroxidation. © 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.orgen_US
dc.relation.ispartofCardiovascular Researchen_US
dc.subject.meshAgingen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntioxidants - Metabolism - Therapeutic Useen_US
dc.subject.meshDisease Susceptibilityen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardial Ischemia - Metabolismen_US
dc.subject.meshMyocardial Reperfusion Injury - Prevention & Controlen_US
dc.subject.meshMyocardium - Metabolismen_US
dc.subject.meshOxidants - Pharmacologyen_US
dc.subject.meshPerfusionen_US
dc.subject.meshPropofol - Metabolism - Therapeutic Useen_US
dc.subject.meshRandom Allocationen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshThiobarbituric Acid Reactive Substances - Analysisen_US
dc.subject.meshTert-Butylhydroperoxide - Pharmacologyen_US
dc.titlePropofol enhances ischemic tolerance of middle-aged rat hearts: Effects on 15-F2t-isoprostane formation and tissue antioxidant capacityen_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.doi10.1016/S0008-6363(03)00351-1en_US
dc.identifier.pmid12829182en_US
dc.identifier.scopuseid_2-s2.0-0038143236en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0038143236&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume59en_US
dc.identifier.issue1en_US
dc.identifier.spage113en_US
dc.identifier.epage121en_US
dc.identifier.isiWOS:000184221300014-
dc.publisher.placeUnited Kingdomen_US

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