[The role of the endothelia in hemostasis]

Unless associated with endothelial lesions or dysfunction, the increased plasma levels of fibrinogen, clotting factors VII and X as well as of fibrin stabilizing factor XIII and of the inhibitors of fibrinolysis, displayed by hyperlipidemic patients, could explain neither the localization nor the mechanisms triggering thrombotic events. Actually, endothelia are provided with both prohemostatic factors (tissue factor, von Willebrand factor, platelet activating factor) and antithrombotic mechanisms (tissue factor pathway inhibitor, proteoglycans activating antithrombin III, thrombodulin activating the protein C system as well as prostacyclin inhibiting platelet aggregation). Endothelia also modulate fibrinolytic activity by producing both activators and inhibitors of plasminogen activation. Evidence was provided that proinflammatory cytokines, anion superoxide and oxidized LDL would cause an upregulation of prohemostatic mechanisms, while down regulating the antithrombotic ones. Attempts made to detect endothelial dysfunction by methods available to the clinical laboratory and author's own observations concerning the behaviour of endothelia-derived plasma von Willebrand factor in various pathological conditions are briefly presented.