Studies on the Pathogenesis of Splenic Anemia

Splenomegaly was produced in rats by repeated intraperitoneal injections of methylcellulose. Anemia and marked reticulocytosis resulted. Coombs tests were negative.

Comparative measurements of red cell life with Cr⁵¹ in normal, methyl-cellulose treated, and splenectomized animals showed a marked decrease of red cell survival in the methylcellulose rats. Slight but statistically insignificant increased survival could be demonstrated in the splenectomized animals.

Excessive red cell destruction occurred in the spleen as evidenced by rapid localization of Cr⁵¹-tagged cells in this organ. Direct correlation between severity of hemolysis and splenic size could be demonstrated. The hemolytic process decreased significantly after splenectomy.

Affected spleens showed red cell congestion of the pulp microscopically. Hemochromogen determinations revealed approximately twice the normal amount of hemoglobin per unit splenic mass.

Quantitative measurements of splenic phagocytosis showed a marked increases of total phagocytic mass with no significant increase of phagocytes per unit of spleen mass.

The mechanism of splenic anemia in these animals is thought to be a combination of an enlarged pulp compartment with resultant stasis and cell destruction.

Methylcellulose-induced splenomegaly may be considered as an experimental model for the study of the hyperfunctional spleen in human disease.