title: Failure of chronic, high-dose, oral vitamin E treatment to protect the ischemic, reperfused porcine heart.
abstract: Lipid peroxidation, presumably the result of free radical-mediated injury, has been shown to occur during myocardial ischemia and reperfusion. Since vitamin E is a very effective, naturally occurring, chain-breaking antioxidant, it was investigated whether a vitamin E-supplemented diet increased myocardial tolerance towards ischemia and reperfusion in pigs. In addition to a standard diet which contained 30 mg vitamin E/kg (approximately daily vitamin E intake 30 mg), ten pigs were fed with 10 g vitamin E (all-rac-alpha-tocopherol acetate, Merck AG, Darmstadt, Germany) daily for at least 4 weeks. Ten control pigs remained on the standard diet. In an open chest preparation, the left anterior descending coronary artery was distally ligated for 45 min followed by 3 d of reperfusion. Infarct size was determined as the ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). Regional systolic shortening was evaluated by sonomicrometry. Vitamin E concentrations in plasma and myocardium were measured by high-performance liquid chromatography. Global hemodynamic characteristics did not differ between the two groups. Oral pretreatment with vitamin E raised the plasma concentration of this vitamin from 1.1 +/- 0.3 to 5.0 +/- 1.0 mg/l and the myocardial content from 4.2 +/- 0.7 to 18.6 +/- 2.7 ng/mg fresh weight. Vitamin E treatment did not reduce infarct size, which amounted to 71.3 +/- 5% in the control group and to 71.7 +/- 8.2% in the treated animals. Furthermore, recovery of regional systolic shortening of the reperfused segment did not significantly differ in the two groups after 3 d of reperfusion; it measured 2 +/- 4% in the controls and 6 +/- 6% (p = 0.16) in the treated animals. Therefore, chronic, oral treatment with vitamin E which raised myocardial and plasma concentrations of this vitamin 4- to 5-fold did not increase myocardial tolerance towards ischemia and reperfusion in this animal model.
authors.affiliation: Department of Cardiology, University of Göttingen, FRG.
authors.forename: H H
authors.initials: HH
authors.lastname: Klein
authors.forename: S
authors.initials: S
authors.lastname: Pich
authors.forename: S
authors.initials: S
authors.lastname: Lindert-Heimberg
authors.forename: K
authors.initials: K
authors.lastname: Nebendahl
authors.forename: P
authors.initials: P
authors.lastname: Niedmann
mesh_terms: D000284:Administration, Oral; D000818:Animals; D003971:Diastole / Q000187:drug effects; D005260:Female; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D013552:Swine; D013599:Systole / Q000187:drug effects; D014810:Vitamin E / Q000008:administration & dosage / Q000378:metabolism / Q000627:therapeutic use*
chemical_list: D014810:Vitamin E