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Table of Contents
Vol. 15, No. 6, 2005
Issue release date: July 2005
Section title: Review
Cell Physiol Biochem 2005;15:245–250

The Negative Regulation of Red Cell Mass by Neocytolysis: Physiologic and Pathophysiologic Manifestations

Rice L. · Alfrey C.P.
Hematology/Oncology Section, Department of Medicine, Baylor College of Medicine, Houston
email Corresponding Author

Lawrence Rice, M.D.

MS 902-Main, Rm 930, 6565 Fannin

Houston, TX 77030 (USA)

Tel. +1/713 441 2127, Fax: +1/713 790 0828

E-Mail lrice@bcm.tmc.edu

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We have uncovered a physiologic process which negatively regulates the red cell mass by selectively hemolyzing young circulating red blood cells. This allows fine control of the number of circulating red blood cells under steady-state conditions and relatively rapid adaptation to new environments. Neocytolysis is initiated by a fall in erythropoietin levels, so this hormone remains the major regulator of red cell mass both with anemia and with red cell excess. Physiologic situations in which there is increased neocytolysis include the emergence of newborns from the hypoxic uterine environment and the descent of polycythemic high-altitude dwellers to sea level. The process first became apparent while investigating the mechanism of the anemia that invariably occurs after spaceflight. Astronauts experience acute central plethora on entering microgravity resulting in erythropoietin suppression and neocytolysis, but the reduced blood volume and red cell mass become suddenly maladaptive on re-entry to earth’s gravity. The pathologic erythropoietin deficiency of renal disease precipitates neocytolysis, which explains the prolongation of red cell survival consistently resulting from erythropoietin therapy and points to optimally efficient erythropoietin dosing schedules. Implications should extend to a number of other physiologic and pathologic situations including polycythemias, hemolytic anemias, ‘blood-doping’ by elite athletes, and oxygen therapy. It is likely that erythropoietin influences endothelial cells which in turn signal reticuloendothelial phagocytes to destroy or permit the survival of young red cells marked by surface molecules. Ongoing studies to identify the molecular targets and cytokine intermediaries should facilitate detection, dissection and eventual therapeutic manipulation of the process.

© 2005 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Review

Published online: June 01, 2005
Issue release date: July 2005

Number of Print Pages: 6
Number of Figures: 0
Number of Tables: 0

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

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