The physiopathology of venous symptoms, such as pain, leg heaviness or swelling sensations, in chronic venous disease (CVD) remains unclear. Localized release of proinflammatory mediators appears to play a key role but the presence of nociceptors sensitive to inflammatory mediators, such as unmyelinated C fibres, needs to be demonstrated. The present study included 10 patients with documented CVD who underwent surgery for saphenectomy.
View Article and Find Full Text PDFClin Hemorheol Microcirc
November 2007
Pain intensity in chronic venous disease varies with the stage in the clinical-etiologic-anatomic-pathophysiologic (CEAP) classification but also with patient perception, pain being by definition subjective. The venous hypertension responsible for the varicose veins and trophic changes in CVD has a variety of algogenic repercussions in which leukocytes play a particular role, notably through their ability to roll along the vessel wall. Shear stress, hypoxia and stasis activate the marginated leukocytes to shed L-selectin from their surface and express integrins, matrix metalloproteinase 9, elastase, lactoferrin and free radicals.
View Article and Find Full Text PDFClin Hemorheol Microcirc
January 2006
Under the influence of heart and elasticity of arteries, circulating blood constantly acts upon the layers of the vessels, covered by active endothelial cells. The shear stress appears like the most efficient mechanical factor developing a rubbing physical force, the laminar flow. But pulsating and centrifugal forces allow shear to be often unsteady.
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