Accessory spleens i n 2 separate necropsy series of (a) 1848 randombred rabbits and @) 21,802 inbred and partially inbred and 880 hybrid rabbits were described and illustrated. The overall frequency in the randombred population (8.9 %) was comparable to that in unselected human necropsy series (10%). The predominant locations of accessory spleens in the rabbits (adjacent to the splenic hilus, the gastrosplenic ligament, and the tail of the pancreas) arranged in descending order, were comparable to their locations in human beings. The inbred rabbits had an overall frequency of at least one accessory spleen of 22.5%, similarly located, and ranged from 1-50%, depending on the strain. It was shown by crosses of high-and low-frequency strains that the presence of accessory spleens is due in part to genetic factors and that a high frequency of accessory spleens is probably a recessive characteristic. The latter interpretation is also supported by the fact that the low or "normal" strains had a n overall frequency of at least 1 accessory spleen of 8.8% which is in accord with both the randombred rabbit population and human necropsy findings.
Analysis of several inbred strains of rabbits with high ( 3 0 5 0 % ) frequencies of accessory spleens revealed that hereditary hematological diseases, autoimmune hemolytic anemia and lymphosarcoma, occurred in some of them. Twenty-one per cent of individuals in these strains, though phenotypically normal, had globulin-coated (Coombs'-positive) erythrocytes. These findings supported observations of increased frequency of accessory spleens in human beings with similar diseases (e.g., autoimmune hemolytic anemia, idiopathic thrombocytopenic purpura, "secondary hypersplenism," Gaucher's disease, hereditary spherocytosis, etc.) and suggested that accessory spleens represent physiological responses to demand for phagocytic capacity provided by the reticuloendothelial system in the spleen, rather than as passive developmental anomalies. This hypothesis predicted that simulation of the basic defect might yield a laboratory model for the induction and study of accessory spleens in rabbits. Phenylhydrazine was used for this purpose and it was shown that the frequency of accessory spleens
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