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dc.contributor.authorDu Toit, EF
dc.contributor.authorSmith, W
dc.contributor.authorMuller, C
dc.contributor.authorStrijdom, H
dc.contributor.authorStouthammer, B
dc.contributor.authorWoodiwiss, AJ
dc.contributor.authorNorton, GR
dc.contributor.authorLochner, A
dc.date.accessioned2017-05-03T15:31:51Z
dc.date.available2017-05-03T15:31:51Z
dc.date.issued2008
dc.date.modified2011-10-17T07:26:02Z
dc.identifier.issn0363-6135
dc.identifier.doi10.1152/ajpheart.00481.2007
dc.identifier.urihttp://hdl.handle.net/10072/26729
dc.description.abstractWe assessed the myocardial susceptibility to ischemic-reperfusion injury in obese rat hearts in the absence and the presence of predicted circulating concentrations of insulin and fatty acids. Feeding rats a high-calorie diet resulted in increases in body weight, visceral fat content, cardiac hypertrophy, plasma insulin, nonesterified free fatty acid, and triglyceride concentrations. In the absence of both insulin and fatty acids in the coronary perfusate, the hearts of obese rats developed an increased infarct size (41.9 ᠱ.9% for obese vs. 22.9 ᠲ.3% for control, P < 0.05) and a reduced percent recovery of aortic output (4.2 ᠴ.2% for obese vs. 27.7 ᠳ.4% for controls, P < 0.05) after coronary artery occlusion and reperfusion. In the presence of insulin in the coronary perfusate, a cardioprotective effect was noted in both groups, an action that was greater in hearts from obese compared with control rats and which abolished the obesity-induced changes in infarct size (13.8 ᠱ.2% for controls vs. 21.0 ᠱ.6% for obese), and percent recovery of aortic output (60.2 ᠴ.7% for controls vs. 45.7 ᠹ.4% for obese). Fatty acids (0.7 mM, control; and 1.5 mM, obese) added to the coronary perfusate with in vivo concentrations of insulin dramatically increased infarct size (48.2 ᠳ.1% for obese, and 37.5 ᠲ.7% for control; P < 0.05 vs. without fatty acids) and decreased percent aortic output recovery (control, 10.4 ᠵ.2%, and obese 7.8 ᠳ.5%; P < 0.05 vs. without fatty acids) in both groups to similar values. In conclusion, in obesity, the impact of an increased susceptibility of the myocardium to ischemic-reperfusion injury on myocardial injury is likely to be overshadowed by the comparatively greater roles played by predicted increases in circulating insulin and fatty acids found in vivo. These data support the notion that adiposity per se is unlikely to be a valuable predictor of outcomes in ischemic-reperfusion injury.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherAmerican Physiological Society
dc.publisher.placeBethesda, USA.
dc.publisher.urihttp://ajpcon.physiology.org/
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefromH2336
dc.relation.ispartofpagetoH2343
dc.relation.ispartofjournalAmerican Journal of Physiology
dc.relation.ispartofvolume294
dc.rights.retentionY
dc.subject.fieldofresearchCardiology (incl. Cardiovascular Diseases)
dc.subject.fieldofresearchPhysiology
dc.subject.fieldofresearchMedical Physiology
dc.subject.fieldofresearchcode110201
dc.subject.fieldofresearchcode0606
dc.subject.fieldofresearchcode1116
dc.titleMyocardial susceptibility to ischemic-reperfusion injury in a prediabetic model of dietary-induced obesity
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.
gro.date.issued2008
gro.hasfulltextNo Full Text
gro.griffith.authorDu Toit, Eugene


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