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e-Article

Blood rheology as a marker of venous hypertension in patients with venous disease.
Document Type
Article
Source
Clinical Hemorheology & Microcirculation. 2004, Vol. 30 Issue 3-4, p307-312. 6p.
Subject
*HEMORHEOLOGY
*HEMODYNAMICS
*HYPERTENSION
*VENOUS insufficiency
*BLOOD circulation disorders
*BLOOD viscosity
Language
ISSN
1386-0291
Abstract
During chronic venous insufficiency (CVI), several microvascular functional abnormalities, due to venous hypertension, develop. To look for blood rheological consequences of venous hypertension “VH”, whole blood viscosity and its main determinants were measured in 11 normal controls and 36 patients with CVI exposed to a short‐term experimental VH. Patients were subdivided into 2 groups according to the severity of their disease. Blood was taken from a foot vein before and after VH, which was induced by appling a pneumatic tourniquet to 100 mmHg for 15 minutes. Whole blood viscosity at low and high shear rates, red blood cell (RBC) aggregation, RBC rigidity, plasma viscosity and proteins as well as red and white blood cell (WBC) counts were recorded. Patients at baseline, i.e., before application of the tourniquet, showed several hemorheological abnormalities such as an increased RBC aggregation, increased low shear rate viscosity, and a significant elevation in plasma fibrinogen level. Patients with more severe CVI had more marked hemorheological changes. The short term VH in patients led to further aggravation of these changes. There were also at baseline lower values, however not significantly, of hematocrit and RBC count, suggesting that hemoconcentration is not a feature of CVI. These same parameters were slightly, however not significantly, increased after VH, indicating a fluid escape into the extravascular space. A significant fall in WBC count was also observed after VH, in keeping with the white cell trapping hypothesis. In conclusion, even a short‐term VH is able to induce several hemorheological impairments, which are probably involved in the failure of the microcirculation and hence the initiation of tissue damage in patients with CVI. [ABSTRACT FROM AUTHOR]