964 RADIATION BIOLOGY 



cytes does not protect rats against radiation damage (Campbell and 

 Ross, 1952). Although transplants of bone marrow do not influence 

 recovery appreciably in dogs (Rekers, 1949; Rekers et al., 1950) and rats 

 (Talbot and Pinson, 1951), intravenous or intraperitoneal administration 

 to certain species is highly effective and, in fact, heterologous marrow 

 (guinea pig to mouse) has considerable effectiveness (Lorenz et al., 1951, 

 1952). The latter does not necessarily implicate a humoral substance 

 since it has been shown that normal tissue can survive and proliferate in 

 an X-irradiated heterologous host (Toolan, 1951). 



The transient granulocytosis that occurs in the rabbit, chicken, and 

 rat during the first hours after X irradiation has been attributed to the 

 mobilization of granulocytes from storage depots as part of the early 

 reaction to injury rather than to a primary stimulation of blood formation 

 (Bloom and Jacobson, 1948). Accelerated maturation of myeloid cells 

 has been noted, however, in the bone marrow of rats during the first 

 hours after total-body irradiation (Rosenthal, Pickering, and Gold- 

 schmidt, 1950). The heterophils or granulocytes are the only circulating 

 cells that are initially increased in number; monocytes and eosinophils, 

 as well as lymphocytes, platelets, and reticulocytes, are invariably 

 reduced. An "abortive rise" of heterophils, lymphocytes, and reticulo- 

 cytes followed by a decline has been observed about one week after acute 

 exposure to X rays or neutrons (Jacobson and Marks, 1946; Jacobson 

 et al, 1947; Jacobson, Marks, and Lorenz, 1949). There is no satis- 

 factory explanation of this phenomenon. 



Hemoglobin concentration and hematocrit, in general, parallel the 

 changes in erythrocyte count. The anemia is, therefore, usually normo- 

 cytic and normochromic (Jacobson, Marks, and Lorenz, 1949). A macro- 

 cytic anemia has been described in the rat after median lethal exposure to 

 X radiation (Steamer et al., 1947a), and similar anemias have been seen 

 in man after poisoning with radioactive materials (Martland, 1926). 

 While radiation-induced anemia is due primarily to the cessation of 

 erythrocyte formation, extravasation of red cells and secondary damage 

 are also substantial factors in its pathogenesis. The role of anemia in 

 acute death occurring within two to three weeks after median lethal 

 irradiation is not clear. The degree of the anemia indicates that it is at 

 most of contributory significance during this period. Anemia may 

 become a critical factor in the deaths seen at later periods, sometimes 

 after a single exposure but more often after repeated irradiation. 



The sedimentation rate of blood is increased after exposure to neutron 

 or X radiation or the injection of Sr 89 or Pu 239 (Prosser, Painter, Lisco, 

 et al, 1947; Ross and Ely, 1947). The increase in sedimentation can be 

 attributed only in small part to the decreased hematocrit and, therefore, 

 is most likely related to some unknown factor in the plasma (Prosser, 

 Painter, Lisco, et al., 1947). The evidence indicates that this is probably 



