The interaction of the time factor and the grouping factor also proved to be significant (p = 0.0318). Using a two-way repeated measures analysis of variance (ANOVA) to examine the effects of vitamin E on FMD, we found no effect for the grouping factor (p = 0.5834) in the ANOVA over time but a highly significant difference with respect to time (p = 0.0065). At the end of the treatment period, a third scan was obtained 20 min after smoking a cigarette (0.6 mg nicotine, 7 mg tare) to estimate transient impairment of FMD.įlow mediated vasodilation at baseline was abnormal in the vitamin E (5.3 ± 3.8, p < 0.01) and in the placebo group (6.4 ± 3.5, p < 0.05) compared with nonsmoking controls (11.6 ± 4.7). Subjects stopped smoking 2 h before the ultrasound examinations. Flow mediated vasodilation and endothelium-independent, nitroglycerin-induced dilation were assessed in the brachial artery using high resolution ultrasound (7.5 MHz) at baseline and after therapy. We studied 22 healthy male smokers (mean ± SD, 23 ± 9 cigarettes per day) randomly assigned to receive either 600 IU vitamin E per day (n = 11, age 28 ± 6 years) or placebo (n = 11, age 27 ± 6 years) for four weeks and 11 age-matched healthy male nonsmokers. Transient impairment of endothelial function after heavy cigarette smoking and chronic endothelial dysfunction in smokers result at least in part from increased oxidative stress.
The aims of this study were to determine whether chronic or acute impairment of flow mediated vasodilation (FMD) in the brachial artery of smokers can be restored or preserved by the antioxidant vitamin E.
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