title: Secondary polycythemia: a boon or a burden?
abstract: The development of a secondary erythrocytosis is usually considered a compensatory effort to counteract tissue hypoxia. However, the associated increase in viscosity tends to decrease blood flow and in theory should augment rather than relieve tissue hypoxia. Clinical observations have supported this concern and phlebotomies have been used to treat cardiopulmonary patients with high hematocrits and to prepare acclimatized mountain climbers for strenuous exercises. Direct measurements of tissue tension in rats and mice have shown that a moderate increase in hematocrit does increase the tissue tension of oxygen, probably due to a concomital increase in blood volume, and only severe increases in hematocrit are detrimental. In contrast, it was found that erythropoietin production in mice and man is decreased at even the most extreme hematocrits, suggesting that the tissue tension in the kidneys is not affected by high hematocrits and sluggish blood flow. This lack of renal hypoxia at high blood viscosities appears to serve an important purpose by preventing a vicious circle in which hypoxia will cause erythrocytosis leading to more hypoxia and more erythrocytosis and so on. However, well maintained secondary erythrocytosis cannot always be considered optimal for overall oxygen transport and has to be evaluated clinically for its potential benefit or harm.
mesh_terms: D000818:Animals; D001809:Blood Viscosity; D004921:Erythropoietin / Q000032:analysis; D006400:Hematocrit; D006801:Humans; D000860:Hypoxia / Q000097:blood / Q000150:complications*; D007668:Kidney / Q000032:analysis; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D011086:Polycythemia / Q000097:blood / Q000209:etiology*; D051381:Rats; D012039:Regional Blood Flow
chemical_list: D004921:Erythropoietin; D010100:Oxygen