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In Vitro Model of Physiological and Pathological Blood Flow with Application to Investigations of Vascular Cell Remodeling
Published on: November 3, 2015
Molecular biology and self-regulatory mechanisms of blood viscosity: a review
1Department of Internal Medicine, Kantonsspital, Chur, Switzerland. walter.reinhart@ksc.gr.ch
Blood viscosity is determined by plasma viscosity, hematocrit, erythrocyte deformability and aggregation. Plasma viscosity and hematocrit are directly regulated by the organism. The molecular biology of the principal determinants of plasma viscosity, i.e., fibrinogen, immunoglobulins, albumin, and lipoproteins is outlined in this work. Hematocrit is regulated by erythropoietin, which is primarily induced by tissue hypoxia. Evidence begins to emerge that autoregulatory mechanisms may be involved in blood viscosity. Viscosity modulates gene transcription for albumin and apolipoproteins in cultured hepatocytes and the erythropoietin response to anemia in rats. Further investigations into these self-regulatory mechanisms in biorheology are, however, needed for a better understanding of blood viscosity regulation in health and disease.
Blood viscosity is determined by plasma viscosity, hematocrit, erythrocyte deformability and aggregation. Plasma viscosity and hematocrit are directly regulated by the organism. The molecular biology of the principal determinants of plasma viscosity, i.e., fibrinogen, immunoglobulins, albumin, and lipoproteins is outlined in this work. Hematocrit is regulated by erythropoietin, which is primarily induced by tissue hypoxia. Evidence begins to emerge that autoregulatory mechanisms may be involved in blood viscosity. Viscosity modulates gene transcription for albumin and apolipoproteins in cultured hepatocytes and the erythropoietin response to anemia in rats. Further investigations into these self-regulatory mechanisms in biorheology are, however, needed for a better understanding of blood viscosity regulation in health and disease.
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