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Updated: Aug 16, 2026

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
[Hemorheological alterations in hypertensive patients]
Patricia Foresto1, Mabel D'Arrigo, Fernando Filippini
1Departamento de Bioquímica Clínica, Facultad de Ciencias Bioquímicas y Farmacéuticas (Instituto de Física CONICET-UNR). pforesto@arnet.com.ar
The aim of this study was to investigate the blood viscosity profile and to evaluate the influence of plasmatic (fibrinogen) and cellular (erythrocyte aggregation) factors in a group of hypertensive patients, compared with a normotensive group. We worked with anticoagulated blood of both non diabetic hypertensive patients (n=31), and healthy individuals (n=40). The plasmatic viscosity and whole blood determination were obtained with a cone-plate viscometer. Erythrocyte aggregation was studied by microscopical observation and quantified by an Aggregate Shape Parameter (ASP), defined as the relation projected area/perimeter. Fibrinogen was determined by the Clauss method with a coagulometer. A comparison between these groups led us to assert that whole blood viscosity was significantly higher in hypertensive patients than in the controls at all shear rates. Plasma viscosity values only showed significant differences between both groups at low shear rate (1.15 a 11.56 seg(-1)). The hypertensive patients showed irregular and amorphous aggregates so that ASP appeared significantly higher (p< 0.001) in patients with hypertension (0.69 +/- 0.11) than in healthy subjects (0.25 +/- 0.12). Fibrinogen appeared slightly higher (p<0.01) in the hypertensive group than in the normal group. Several hemorheological parameters play important roles in the pathogenesis of hypertension. Among these factors, several hemorheological parameters could be altered in hypertension (hematocrit, plasma fibrinogen level, erythrocyte deformability and aggregability, plasma and whole blood viscosity). An increased RBC aggregation has been identified as an important factor responsible for disturbing blood rheological behavior in the microcirculation. The present study demonstrates an abnormal erythrocyte aggregation, which was detected by increased ASP values that could be responsible for vascular complications in hypertension.
The aim of this study was to investigate the blood viscosity profile and to evaluate the influence of plasmatic (fibrinogen) and cellular (erythrocyte aggregation) factors in a group of hypertensive patients, compared with a normotensive group. We worked with anticoagulated blood of both non diabetic hypertensive patients (n=31), and healthy individuals (n=40). The plasmatic viscosity and whole blood determination were obtained with a cone-plate viscometer. Erythrocyte aggregation was studied by microscopical observation and quantified by an Aggregate Shape Parameter (ASP), defined as the relation projected area/perimeter. Fibrinogen was determined by the Clauss method with a coagulometer. A comparison between these groups led us to assert that whole blood viscosity was significantly higher in hypertensive patients than in the controls at all shear rates. Plasma viscosity values only showed significant differences between both groups at low shear rate (1.15 a 11.56 seg(-1)). The hypertensive patients showed irregular and amorphous aggregates so that ASP appeared significantly higher (p< 0.001) in patients with hypertension (0.69 +/- 0.11) than in healthy subjects (0.25 +/- 0.12). Fibrinogen appeared slightly higher (p<0.01) in the hypertensive group than in the normal group. Several hemorheological parameters play important roles in the pathogenesis of hypertension. Among these factors, several hemorheological parameters could be altered in hypertension (hematocrit, plasma fibrinogen level, erythrocyte deformability and aggregability, plasma and whole blood viscosity). An increased RBC aggregation has been identified as an important factor responsible for disturbing blood rheological behavior in the microcirculation. The present study demonstrates an abnormal erythrocyte aggregation, which was detected by increased ASP values that could be responsible for vascular complications in hypertension.
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