File Download
  • No File Attached
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Propofol enhances ischemic tolerance of middle-aged rat hearts: Effects on 15-F2t-isoprostane formation and tissue antioxidant capacity
  • Basic View
  • Metadata View
  • XML View
TitlePropofol enhances ischemic tolerance of middle-aged rat hearts: Effects on 15-F2t-isoprostane formation and tissue antioxidant capacity
 
AuthorsXia, Z1
Godin, DV1
Ansley, DM1
 
Issue Date2003
 
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
 
CitationCardiovascular Research, 2003, v. 59 n. 1, p. 113-121 [How to Cite?]
DOI: http://dx.doi.org/10.1016/S0008-6363(03)00351-1
 
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.
 
ISSN0008-6363
2013 Impact Factor: 5.808
2013 SCImago Journal Rankings: 2.799
 
DOIhttp://dx.doi.org/10.1016/S0008-6363(03)00351-1
 
ISI Accession Number IDWOS:000184221300014
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorXia, Z
 
dc.contributor.authorGodin, DV
 
dc.contributor.authorAnsley, DM
 
dc.date.accessioned2012-05-29T06:00:45Z
 
dc.date.available2012-05-29T06:00:45Z
 
dc.date.issued2003
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationCardiovascular Research, 2003, v. 59 n. 1, p. 113-121 [How to Cite?]
DOI: http://dx.doi.org/10.1016/S0008-6363(03)00351-1
 
dc.identifier.doihttp://dx.doi.org/10.1016/S0008-6363(03)00351-1
 
dc.identifier.epage121
 
dc.identifier.isiWOS:000184221300014
 
dc.identifier.issn0008-6363
2013 Impact Factor: 5.808
2013 SCImago Journal Rankings: 2.799
 
dc.identifier.issue1
 
dc.identifier.pmid12829182
 
dc.identifier.scopuseid_2-s2.0-0038143236
 
dc.identifier.spage113
 
dc.identifier.urihttp://hdl.handle.net/10722/147202
 
dc.identifier.volume59
 
dc.languageeng
 
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofCardiovascular Research
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAging
 
dc.subject.meshAnimals
 
dc.subject.meshAntioxidants - Metabolism - Therapeutic Use
 
dc.subject.meshDisease Susceptibility
 
dc.subject.meshMale
 
dc.subject.meshMyocardial Ischemia - Metabolism
 
dc.subject.meshMyocardial Reperfusion Injury - Prevention & Control
 
dc.subject.meshMyocardium - Metabolism
 
dc.subject.meshOxidants - Pharmacology
 
dc.subject.meshPerfusion
 
dc.subject.meshPropofol - Metabolism - Therapeutic Use
 
dc.subject.meshRandom Allocation
 
dc.subject.meshRats
 
dc.subject.meshRats, Sprague-Dawley
 
dc.subject.meshThiobarbituric Acid Reactive Substances - Analysis
 
dc.subject.meshTert-Butylhydroperoxide - Pharmacology
 
dc.titlePropofol enhances ischemic tolerance of middle-aged rat hearts: Effects on 15-F2t-isoprostane formation and tissue antioxidant capacity
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Xia, Z</contributor.author>
<contributor.author>Godin, DV</contributor.author>
<contributor.author>Ansley, DM</contributor.author>
<date.accessioned>2012-05-29T06:00:45Z</date.accessioned>
<date.available>2012-05-29T06:00:45Z</date.available>
<date.issued>2003</date.issued>
<identifier.citation>Cardiovascular Research, 2003, v. 59 n. 1, p. 113-121</identifier.citation>
<identifier.issn>0008-6363</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/147202</identifier.uri>
<description.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 &#956;g/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 &#956;l/min. Propofol in KH was perfused at 12 &#956;g/ml for the first 15 min of reperfusion and subsequently reduced to 5 &#956;g/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&lt;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. &#169; 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved.</description.abstract>
<language>eng</language>
<publisher>Oxford University Press. The Journal&apos;s web site is located at http://cardiovascres.oxfordjournals.org</publisher>
<relation.ispartof>Cardiovascular Research</relation.ispartof>
<subject.mesh>Aging</subject.mesh>
<subject.mesh>Animals</subject.mesh>
<subject.mesh>Antioxidants - Metabolism - Therapeutic Use</subject.mesh>
<subject.mesh>Disease Susceptibility</subject.mesh>
<subject.mesh>Male</subject.mesh>
<subject.mesh>Myocardial Ischemia - Metabolism</subject.mesh>
<subject.mesh>Myocardial Reperfusion Injury - Prevention &amp; Control</subject.mesh>
<subject.mesh>Myocardium - Metabolism</subject.mesh>
<subject.mesh>Oxidants - Pharmacology</subject.mesh>
<subject.mesh>Perfusion</subject.mesh>
<subject.mesh>Propofol - Metabolism - Therapeutic Use</subject.mesh>
<subject.mesh>Random Allocation</subject.mesh>
<subject.mesh>Rats</subject.mesh>
<subject.mesh>Rats, Sprague-Dawley</subject.mesh>
<subject.mesh>Thiobarbituric Acid Reactive Substances - Analysis</subject.mesh>
<subject.mesh>Tert-Butylhydroperoxide - Pharmacology</subject.mesh>
<title>Propofol enhances ischemic tolerance of middle-aged rat hearts: Effects on 15-F2t-isoprostane formation and tissue antioxidant capacity</title>
<type>Article</type>
<description.nature>Link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1016/S0008-6363(03)00351-1</identifier.doi>
<identifier.pmid>12829182</identifier.pmid>
<identifier.scopus>eid_2-s2.0-0038143236</identifier.scopus>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-0038143236&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>59</identifier.volume>
<identifier.issue>1</identifier.issue>
<identifier.spage>113</identifier.spage>
<identifier.epage>121</identifier.epage>
<identifier.isi>WOS:000184221300014</identifier.isi>
<publisher.place>United Kingdom</publisher.place>
</item>
Author Affiliations
  1. The University of British Columbia