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PubMed · 4058620

Why the kidney?

A J Erslev·J Caro·A Besarab
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Abstract

Severe erythrocytosis is associated with increased whole blood viscosity and impaired blood flow. Since a reduced blood flow will cause tissue hypoxia and since tissue hypoxia is associated with increased synthesis of erythropoietin, erythrocytosis per se should cause an increase in the rate of red cell production. This, however, does not occur and severe erythrocytosis in patients with polycythemia vera does not lead to increased synthesis of erythropoietin. We propose here that the reason for this discrepancy is that decreased blood flow to the kidneys, the site of erythropoietin synthesis, does not cause renal tissue hypoxia. The oxygen tension in the kidneys is to a great extent determined by the consumption of oxygen used for sodium reabsorption and since sodium reabsorption is roughly proportional to glomerular filtration, a decreased flow of blood should be matched by a decreased oxygen consumption leaving the tissue tension of oxygen unchanged. Consequently, the location of an oxygen sensor in the kidneys controlling erythropoietin production appears to be most fortuitous since it prevents the development of a vicious circle, with erythrocytosis causing more erythrocytosis.

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Blood ViscosityErythropoietinGlomerular Filtration RateHematocritHumansHypoxiaKidneyOxygen ConsumptionPolycythemiaPolycythemia VeraRadioimmunoassayRegional Blood FlowSodiumJournal ArticleResearch Support, U.S. Gov't, P.H.S.

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A J Erslev, J Caro, A Besarab. 1985. Why the kidney?. https://doi.org/10.1159/000183585

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PubMed1992

Role of plasma viscosity in platelet adhesion.

Platelet adhesion to the vessel wall is initiated by transport of blood platelets from the bulk flow to the wall. The process of diffusion and convection of the platelets is affected by rheological conditions such as well shear rate, red blood cell (RBC) deformability, and viscosity of the medium. To study the effect of plasma viscosity on platelet adhesion, perfusion experiments with a rectangular perfusion chamber were performed. Reconstituted blood, consisting of washed platelets and washed RBCs, was circulated through this chamber for 5 minutes at a wall shear rate of 300 s-1. Different albumin concentrations were made, to obtain different medium viscosities (0.89 to 1.85 mPa.s). Platelet adhesion decreased with increasing medium viscosity up to viscosities of 0.95 mPa.s, but increased with medium viscosity above this value. Instead of human albumin solution, different plasma viscosities were obtained by dilution of Waldenström plasma with buffer. Plasma was depleted of fibronectin, which gave a final plasma viscosity of 2.0 mPa.s, and was dialyzed against HEPES buffer and subsequently diluted with the dialysis buffer in different fractions (0.89 to 2.00 mPa.s). Perfusions were performed over a purified von Willebrand factor coating on glass, or over an endothelial cell matrix, preincubated with von Willebrand factor. With both surfaces, platelet adhesion was dependent on the plasma viscosity in a similar way: at low plasma viscosities, adhesion was decreased with increasing plasma viscosity, while at higher plasma viscosities, adhesion increased with plasma viscosity. Adhesion values at higher plasma viscosity or at higher human albumin concentrations could be explained by effects of the medium on the rigidity of the RBCs, since platelet adhesion is known to be increased by enhanced RBC rigidity. Effects of the medium on the deformability of the RBCs were measured separately with the laser diffraction method. These experiments confirmed that presence of human albumin or plasma in the measuring suspension increased the rigidity of RBCs. To prevent influence of the medium on the RBCs in perfusion experiments, the RBCs were fixated with glutaraldehyde. Perfusion experiments with fixated RBCs in plasma over a von Willebrand factor preincubated endothelial cell matrix, showed a consequent decrease in adhesion with increasing plasma viscosity, according to the diffusion theories, whereas the increase of adhesion at high plasma viscosities was lacking. This suggests that the latter effect was entirely due to increased transport of platelets by more rigid RBCs.

Blood Viscosity↗