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Varicose Veins: Loss of Release of Vascular Endothelial Growth Factor and Reduced Plasma Nitric Oxide

  • S.J. Hollingsworth
    Affiliations
    The Academic Vascular Unit, Department of Surgery, The Royal Free and University College London Medical School, The Middlesex Hospital, Mortimer Street, London, W1N 8AA, U.K.
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  • C.B. Tang
    Affiliations
    The Academic Vascular Unit, Department of Surgery, The Royal Free and University College London Medical School, The Middlesex Hospital, Mortimer Street, London, W1N 8AA, U.K.
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  • M. Dialynas
    Affiliations
    The Academic Vascular Unit, Department of Surgery, The Royal Free and University College London Medical School, The Middlesex Hospital, Mortimer Street, London, W1N 8AA, U.K.
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  • S.G.E. Barker
    Affiliations
    The Academic Vascular Unit, Department of Surgery, The Royal Free and University College London Medical School, The Middlesex Hospital, Mortimer Street, London, W1N 8AA, U.K.
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      Abstract

      Objectives: to examine the release of vascular endothelial growth factor (VEGF) and nitric oxide (NO) in primary varicose veins (VVs) and normal vein controls following experimentally-induced venous stasis. Design, materials and methods: patients with primary VVs (n=21) and control subjects (n=11) were rested supine for 15 min. Blood was collected from both an arm and foot vein. A below-knee cuff was applied and inflated to 90–95 mmHg for 10 min (to prompt venous stasis). Further blood samples were collected from the foot vein. Levels of plasma VEGF and NO were analysed. Results: in control subjects, application of the cuff increased levels of plasma VEGF in the foot (p<0.025). In contrast, in patients with VVs, there was little or no change in these levels of plasma VEGF. Cuff application had little effect on levels of plasma NO in either controls, or those with VVs. When compared to controls however, the levels of plasma NO in all samples with VVs (arm, or foot before, or after, cuff application) were reduced (all, p<0.05). Conclusions: loss of VEGF release with experimentally-induced venous stasis, and reduced levels of plasma NO may suggest a mechanism important in the development of primary VVs.

      Keywords

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