HEMATOLOGIC EFFECTS OF RADIATION 1039 



at about 9 days if a cessation of erythropoiesis was the only aspect 

 involved. Gross hemorrhage in mice is not a factor under these condi- 

 tions. Microscopic hemorrhage and extensive erythrophagocytosis are 

 constant histopathologic findings after exposure to 1025 r. Both proc- 

 esses culminate in the eventual hemolysis of the involved red cells. (As 

 described later, gross hemorrhage may occasionally be a major factor in 

 the production of an anemia in dogs, pigs, and guinea pigs.) Schwartz 

 et al. (1947) and Lawrence, Dowdy, and Valentine (1948), and others have 

 studied the role of red-cell hemolysis in postirradiation anemia and have 

 found evidence of an increased excretion of the breakdown products of 

 hemoglobin. The increased pigment excretion observed in dogs after 

 exposure to an LD 5 o dose is not of sufficient magnitude to warrant the 

 conclusion that increased erythrocyte hemolysis plays a role in the 

 anemia since an indeterminate number of hemoglobin-containing erythro- 

 cyte precursors are destroyed in situ by irradiation. This may account 

 for the increased pigment excretion. Davis et al. (1950) restudied this 

 problem and found an increase in bile-pigment excretion in dogs exposed 

 to 150-250 r during the first and second weeks after irradiation. No 

 increased erythrocyte fragility (thermal or mechanical) was apparent, 

 however, in these animals. Davis and his co-workers considered the 

 possibility that increased pigment excretion might be based on destruc- 

 tion of the erythrocyte precursors. Prosser et al. (1947) recognized that 

 the changes occurring in circulatory dynamics were masking actual 

 changes in red-cell and hemoglobin levels and that the anemia that 

 eventually developed after exposure of the dog or rabbit to LD 5 o dosages 

 could not be accounted for by cessation of hematopoiesis or hemorrhage 

 and postulated, as have many others (Heineke, 1905; Schwartz et al., 

 1947; Dunlap et al., 1944; Selling and Osgood, 1938), that an abnormal 

 hemolysis of erythrocytes was probably involved. 



Recently Furth and associates (Storey, Wish, and Furth, 1950; Furth 

 et al., 1951; Kahn and Furth, 1952; Ross, Furth, and Bigelow, 1952), 

 using a number of techniques including P 32 and Fe 59 labeling of the red 

 cells and I 131 labeling of the plasma combined with regular hematologic 

 and histopathologic investigation, have clarified many of the problems 

 concerning postirradiation anemia. This work, based on studies of mice, 

 rabbits, and dogs X-irradiated in the LD 5 o range and above, may be 

 summarized as follows: 



1. Erythropoiesis ceases within 24 hours after irradiation and is not 

 resumed for 7-14 days. 



2. During this same period there is a reduction in the red-cell mass as 

 determined by isotopic studies (Fe 59 and P 32 ), and there is a simultaneous 

 decrease in the plasma volume. This change masks the magnitude of the 

 drop in erythrocyte mass, especially during the first postirradiation week, 



