Skip to main content
The Journal of Experimental Medicine logoLink to The Journal of Experimental Medicine
. 1917 May 1;25(5):665–673. doi: 10.1084/jem.25.5.665

THE NORMAL FATE OF ERYTHROCYTES

II. BLOOD DESTRUCTION IN PLETHORIC ANIMALS AND IN ANIMALS WITH A SIMPLE ANEMIA.

Oswald H Robertson 1, Peyton Rous 1
PMCID: PMC2125511  PMID: 19868116

Abstract

1. The increased destruction of red cells in animals rendered plethoric by transfusion takes place predominantly by a fragmentation of the corpuscles without loss of hemoglobin. 2. The microcytes and poikilocytes observed in animals with a severe anemia due to hemorrhage are not put forth as such by the bone marrow, but are portions of cells fragmented while circulating. 3. The cells thus fragmented are for the most part those newformed to meet the exigencies of the situation. Such cells are in large part unable to withstand the wear and tear of function. There results a vicious circle. The anemia renders the bone marrow unable to put forth proper cells, and those it does produce are soon destroyed, thus prolonging the condition. A similar state of affairs probably exists in many human anemias. 4. The occurrence of large accumulations of microcytes and poikilocytes in the spleen of anemic and plethoric animals indicates that the organ exercises some important function in connection with these forms. The same is true of normal animals, for the findings in them are similar, though less striking. 5. The normal fate of the red corpuscles, in those species in which phagocytosis is negligible, is to be fragmented one by one, while still circulating, to a fine, hemoglobin-containing dust. The cell fragments are rapidly removed from the blood, but their ultimate fate remains to be determined. The facts indicate that they are removed from the blood by the spleen, and under exceptional conditions, by the bone marrow.

Full Text

The Full Text of this article is available as a PDF (438.0 KB).


Articles from The Journal of Experimental Medicine are provided here courtesy of The Rockefeller University Press

RESOURCES