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Microvascular Reactivity in Response to Smoking and Oral Antioxidants in Humans
Author(s) -
HENRIKSSON PETER,
DICZFALUSY ULF,
FREYSCHUSS ANNA
Publication year - 2012
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/j.1549-8719.2011.00125.x
Subject(s) - microcirculation , oxidative stress , vitamin c , medicine , antioxidant , ascorbic acid , vitamin e , physiology , blood flow , endocrinology , vitamin , chemistry , biochemistry , food science
Please cite this paper as : Henriksson, Diczfalusy and Freyschuss (2012). Microvascular Reactivity in Response to Smoking and Oral Antioxidants in Humans. Microcirculation 19 (1), 86–93. Abstract Objective: To investigate whether a daily intake of a moderate dose of antioxidants modifies the microcirculatory response to smoking, assuming a major influence of oxidative stress on microcirculation. Methods: The microvascular response to smoking was assessed in individual capillaries by capillaroscopy before and after two weeks of treatment with oral antioxidants. Results: Smoking prolonged time to peak (TtP) capillary blood flow velocity in all subjects. When the subjects were pre‐treated with ascorbate, TtP was comparable to baseline values of untreated subjects. No significant effect of vitamin E was observed either before or after smoking. Capillary blood flow velocity increased after treatment with ascorbate as well as after vitamin E. However, significant reductions in velocity were still observed in response to smoking even after subjects consumed ascorbate and vitamin E ( p < 0.0004 and p < 0.8 respectively). Conclusions: This study focused on individual capillaries, and confirms that smoking has a very pronounced, direct and reproducible microvascular effect possible to demonstrate in vivo in human capillaries. Moderate intake of the antioxidant ascorbate clearly mitigated the effects induced by smoking. TtP after smoking in subjects treated with ascorbate was similar to that observed in untreated subjects before smoking a cigarette. Thus, oxidative stress could be assumed to play a role in the effects of smoking on microcirculation.