Indeed, this field of investigation is expanding rapidly, further clarification of the possible association or dissociation between MS and CCSVI is likely forthcoming. Smoking is reported to be significantly associated with lower limb venous insufficiency. The mechanisms leading to harmful effects of tobacco on the venous system are still not elucidated.127 However, cigarette smoking is believed to be a major factor in hypoxia through carbon monoxide and NO fixation in hemoglobin.127,128 It has been hypothesized that the effect of hypoxia on the functional state of the endothelium can be the starting point of a cascade of events leading to disorganization of the vessel typical of venous pathologies such as varicose veins. Hypoxia activates the endothelial cells, resulting in the production of proinflammatory factors within the vessel wall, increased capillary permeability and local inflammatory changes.129 Endothelial basal lamina has been found thickened in heavy smokers and the thickening contained fibronectin.130 It has also been reported that heavy smokers have impaired release of endothelium-derived relaxing factor in response to bradykinin and calcium ionophore. This impairment may increase vasomotor tone and smooth muscle proliferation in veins.131 Even the implication of a developmental origin in venous anomalies seen in CCSVI132 does not exclude the possibility that smoking could contribute to the venous flow abnormalities. It can thus be speculated that smoking may be related to venous MS hypothesis through harmful effects of tobacco on the venous system and its hemodynamics.
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