Literature DB >> 8441176

Failure of chronic, high-dose, oral vitamin E treatment to protect the ischemic, reperfused porcine heart.

H H Klein1, S Pich, S Lindert-Heimberg, K Nebendahl, P Niedmann.   

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.

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Year:  1993        PMID: 8441176     DOI: 10.1006/jmcc.1993.1011

Source DB:  PubMed          Journal:  J Mol Cell Cardiol        ISSN: 0022-2828            Impact factor:   5.000


  5 in total

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2.  Antioxidant and oxidative stress changes in experimental cor pulmonale.

Authors:  Firoozeh Farahmand; Michael F Hill; Pawan K Singal
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Review 4.  Oxidative stress in congestive heart failure.

Authors:  P K Singal; N Khaper; F Farahmand; A Belló-Klein
Journal:  Curr Cardiol Rep       Date:  2000-05       Impact factor: 3.955

Review 5.  Oxidative stress in cardiovascular diseases and obesity: role of p66Shc and protein kinase C.

Authors:  Elena De Marchi; Federica Baldassari; Angela Bononi; Mariusz R Wieckowski; Paolo Pinton
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  5 in total

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