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The Hemorheologic-Hemodynamic Theory of Atherosclerosis -- Role of Lipoproteins in Atherogenesis (Part 6)

Role of Lipoproteins in Atherogenesis

The hemorheologic-hemodynamic theory predicts that LDL (low-density lipoprotein) should increase blood viscosity and HDL (high-density lipoprotein) should decrease blood viscosity, which has been demonstrated experimentally [1]. Erythrocytes are separated by a minimum intercellular distance of approximately 15 nanometers due to electrostatic repulsion. LDL has a particle diameter of 18 to 40 nanometers, large enough to simultaneously bind to two erythrocytes and form erythrocyte aggregates. These increase blood viscosity at low shear by increasing the mass of the suspended particles. HDL, with a particle diameter of 8 to 12 nanometers, is too small to promote erythrocyte aggregation. Instead, by competing with LDL for binding to erythrocytes, it antagonizes erythrocyte aggregation and decreases blood viscosity. Erythrocyte aggregates are weak, and progressively disrupted with increasing shear, decreasing blood viscosity. Given the relationship of LDL to blood viscosity, it is not surprising that hypercholesterolemia is a risk factor for both atherosclerosis and deep venous thrombosis [2].

Next Section: Insights Provided by the Hemorheologic-Hemodynamic Theory (Part 7)


References:

1. Sloop GD, Garber DW. The effects of low-density lipoprotein and high-density lipoprotein on blood viscosity correlate with their association with risk of atherosclerosis in humans. Clinical Science 1997;92:473-9.

2. Kawasaki T, Kambayashi J, Ariyoshi H, Sakon M, Suehisa E, Monden M. Hypercholesterolemia as a risk factor for deep-vein thrombosis. Thrombosis Research 1997;88:67-73.

ⓒ 2011 Gregory Sloop. All Rights Reserved.

 

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