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Abstract
Following a single subcutaneous dose of acetylphenylhydrazine (APH) to rats, the entire
erythrocyte population was removed by the reticuloendothelial system (RES), primarily
liver and spleen, at a relatively slow rate by largely extravascular mechanisms with
only a modest fall in hematocrit. In this process, erythrocytes were removed at an
increasingly accelerated rate from the blood, suggesting progressive oxidative damage
to the erythrocytes. This category of hemolytic process has not been described previously
in animals or man with a drug induced hemolysis. The spleen was the most important
organ of sequestration and a more sensitive trap for the damaged erythrocytes than
the liver. After labeling the erythrocytes, splenic Fe59 and Cr51 reflected the removal of APH damaged erythrocytes from the blood. The maximum accumulation
of Fe59 and Cr51 in the spleen occurred earlier after a large dose of APH than after a small dose.
However, maximum spleen weights were reached at the same time with both large and
small doses. These facts suggested that splenic hypertrophy was caused by several
factors, one of which was erythrocyte phagocytosis. Chromium-51 from erythrocytes
was avidly retained by the liver and spleen and was lost from treated rats at no greater
rate than from untreated controls for 9 days after APH. Two different doses of APH,
producing entirely different rates of extravascular destruction, resulted in the same
loss of Cr51 from the rats. Reutilization of Fe59 from damaged erythrocytes was not prevented by iron loading, and Fe59 from such cells egressed from the spleen faster than from the liver. Old rat erythrocytes
containing Fe59 were removed from the blood and sequestered in spleen and liver to a greater extent
than young erythrocytes 4 days after APH.
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Article info
Publication history
Accepted:
September 27,
1963
Received:
August 2,
1963
Footnotes
☆Supported by a grant from the United States Public Health Service.
Identification
Copyright
© 1964 Published by Elsevier Inc.
