Literature review reveals that venotropic drugs counter hypoxia-induced endothelial damage via the mitochondrial respiratory chain in venous disease, highlighting a shared therapeutic mechanism.
Objective: To review the literature concerning chronic venous disease of the leg and the mechanisms of action of venotropic drugs.: The authors identified relevant papers from their own collection and from medical literature databases.: Endothelial cell activation caused by exposure to the hypoxic conditions that develop during blood stasis in chronic venous insufficiency patients is proposed to be one factor initiating a pro-inflammatory process in the leg veins. Recruited and activated neutrophils would then be responsible for alterations of the venous wall, typical of what is observed in varicose veins. Venotropic drugs used in the treatment of chronic venous insufficiency patients have long been known to decrease vascular permeability and increase venous tone. Recently, it has been shown that they are also able to prevent endothelial cell activation by hypoxia and a precise biochemical target common to all of them has been identified: the mitochondrial respiratory chain.: The influence of venotropic drugs on the mitochondrial respiratory chain provides a rational explanation for the therapeutic benefit to patients of this class of drugs.
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Michiels et al. (2002) studied this question.
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