Pathological study on experimental Heinz body anemia: intracellular changes of phagocytized red cells in macrophages of the spleen and liver.
Heinz body anemia was experimentally produced in mice by phenylhydrazine injection and the mechanism of hemolysis was investigated. Both in acute and chronic experiments, the "culling" function of the spleen was more important in removing the red cells containing Heinz bodies than the "pitting" function. In addition to extravascular hemolysis, intravascular hemolysis in the spleen, liver and in the peripheral circulation was evident as manifested by the presence of ghost cells and hemosiderin deposition in the kidney. In the absence of the spleen, the liver can replace the function of the spleen to a certain extent and selective removal of Heinz bodies by the Kupffer cell was occasionally demonstrated. Deposition of yellowish-brown pigments was noted in the cordal macrophages and the Kupffer cells, but the precise nature of these pigments is unknown.
D000208:Acute Disease; D000743:Anemia, Hemolytic / Q000473:pathology*; D000818:Animals; D002908:Chronic Disease; D004912:Erythrocytes / Q000648:ultrastructure; D005260:Female; D006366:Heinz Bodies / Q000648:ultrastructure*; D007728:Kupffer Cells / Q000648:ultrastructure; D008099:Liver / Q000648:ultrastructure*; D008264:Macrophages / Q000648:ultrastructure; D008297:Male; D051379:Mice; D010587:Phagocytosis; D012156:Reticulocytes / Q000648:ultrastructure; D013154:Spleen / Q000648:ultrastructure*