Abstract
Chronic occlusive arterial disease has been shown to be accompanied by blood hyperviscosity which is associated with increased plasma viscosity, red cell aggregation and red cell rigidity. There exists a linear correlation between fibrinogen and plasma viscosity and the flow behaviour of red cells meshed to each other by fibrinogen. Therapeutical decrease of the fibrinogen level aims at improving blood fluidity and increasing tissue perfusion by raising blood flow velocity in conjunction with an increase in red cell oxygen transport rate. Pharmacological approaches to realize this therapeutical principal are: fibrinolysis (streptokinase, urokinase, in myocardial infarction); defibrinogenation (ancrod, defibrase, in peripheral vascular disease); anabolics (stanazol in Raynaud’s-Syndrome), lipid lowering drugs (clofibrate analogous in peripheral vascular disease), hemorheologically active drugs (pentoxifylline). Confirmed effects in respect of improvement of blood fluidity and tissue perfusion via fibrinogen reduction are at present only available for defibrinogenation by ancrod and by pentoxifylline.
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