title: Vitamin E deficiency fails to affect myocardial performance during in vivo ischemia-reperfusion.
abstract: Vitamin E content of cardiac tissue has been proposed to play a major role in the damage caused by myocardial ischemia-reperfusion (I-R). Previous studies using in vitro models have examined vitamin E deficiency and I-R-induced myocardial damage with equivocal results. The purpose of this study was to use an in vivo model of myocardial I-R to determine the effects of vitamin E deficiency on myocardial I-R-induced damage. Female Sprague-Dawley rats (4-mo old) were assigned to either: 1) control diet (CON), or 2) vitamin E deficient diet (VE-DEF). The CON diet was prepared to meet AIN-93M standards, which contains 75 IU vitamin E/kg diet. The VE-DEF diet was the AIN-93M diet prepared with tocopherol stripped corn oil and no vitamin E. Following a 14-week feeding period, significant differences (p < 0.05) existed in mean myocardial VE levels between groups (mean values +/- SEM: CON = 48.2 +/- 3.5; VE-DEF = 12.4 +/- 1.4 micrograms VE/g wet weight). Animals from both experimental groups were subjected to an in vivo I-R protocol consisting of 25 minutes of left coronary artery occlusion followed by 10 minutes of reperfusion. No group differences (p > 0.05) existed in cardiac performance (peak arterial pressure or ventricular work) or the incidence of ventricular arrhythmias during the I-R protocol. VE-DEF animals had significantly higher (p < 0.05) levels of myocardial lipid peroxidation and lower (p < 0.05) protein thiols following I-R compared to the CON animals. These data suggest that although vitamin E deficiency increases oxidative damage resulting from myocardial I-R, it does not affect cardiac performance during the insult.
authors.affiliation: School of Human Movement Studies, University of Queensland, St Lucia, Qld., Australia, 4072.
authors.forename: J S
authors.initials: JS
authors.lastname: Coombes
authors.forename: S K
authors.initials: SK
authors.lastname: Powers
authors.forename: H A
authors.initials: HA
authors.lastname: Demirel
authors.forename: K L
authors.initials: KL
authors.lastname: Hamilton
authors.forename: J
authors.initials: J
authors.lastname: Jessup
authors.forename: H K
authors.initials: HK
authors.lastname: Vincent
authors.forename: R A
authors.initials: RA
authors.lastname: Shanely
mesh_terms: D000821:Animal Feed; D000818:Animals; D001555:Benzene Derivatives / Q000032:analysis; D004195:Disease Models, Animal; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D006321:Heart / Q000502:physiology*; D015227:Lipid Peroxidation / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects*; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000737:chemistry*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D016276:Ventricular Function / Q000187:drug effects; D014810:Vitamin E / Q000032:analysis / Q000494:pharmacology* / Q000627:therapeutic use; D014811:Vitamin E Deficiency / Q000150:complications* / Q000503:physiopathology
chemical_list: D001555:Benzene Derivatives; D005609:Free Radicals; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; C007164:cumene hydroperoxide