PHYSIOLOGY OF RADIATION INJURY 963 



two weeks, but several months may elapse before regeneration is com- 

 plete (Bloom and Jacobson, 1948). Overcompensation or secondary 

 aplasia, sometimes seen during the recovery phase, can give rise to blood 

 dyscrasias, which have been encountered especially after repeated irradia- 

 tion. It is well known that a minimal exposure becomes important if 

 repeated frequently enough to result in a significant accumulated dose. 

 Definite hematological changes may appear in guinea pigs after exposure 

 to as little as 1.1 r per day (Lorenz et al., 1946). On the other hand, there 

 is no evidence of any permanent functional impairment of the hemato- 

 poietic tissues when cats are subjected to a whole-body irradiation with 

 200 r every four months over a period of a year and a half (Valentine, 

 Pearce, and Lawrence, 1951). 



From the point of view of the time course of events in peripheral blood, 

 the most important consideration appears to be the rate of utilization or 

 life span of the various cellular elements. This increases progressively 

 from the lymphocyte to the granulocyte, reticulocyte, thrombocyte, and 

 erythrocyte, and represents the order in which changes occur in the 

 peripheral blood after exposure to penetrating radiation in single or 

 divided doses (Lawrence, Dowdy, and Valentine, 1948; Jacobson, Marks, 

 and Lorenz, 1949; Suter, 1947). Significant reduction in the number of 

 lymphocytes has been detected after a single total-body exposure to 25 r. 

 Regeneration, however, does not follow the same pattern since recovery is 

 ordinarily seen first in the reticulocytes, granulocytes, and thrombocytes, 

 then in the erythrocytes and lymphocytes. 



Recovery of hematopoietic tissue is more rapid after subtotal irradia- 

 tion (Boffil and Miletzky, 1946; Jacobson, Simmons, Marks, Gaston, et al., 

 1951; Rekers, 1949). The observations of Jacobson and his colleagues 

 (Jacobson, Marks, Robson, et al., 1949; Jacobson, Simmons, et al., 1950; 

 Jacobson, Simmons, Marks, Gaston, et al., 1951) are of particular sig- 

 nificance in this connection. They have shown that shielding the spleen 

 in mice and rats or the appendix in rabbits lessens the severity of the 

 blood changes and enhances recovery. Splenectomy performed prior to 

 irradiation does not modify the hematologic response to X rays (Steamer 

 et al., 1947b), although it does increase the severity of the anemia that 

 occurs after poisoning with Sr 89 (Jacobson, Simmons, and Block, 1949). 

 Anemia fails to develop when Sr 89 is given to the normal mouse, appar- 

 ently because of the intense ectopic erythropoiesis in the spleen. The 

 mechanism of these protective effects is not understood; it has been 

 suggested (Jacobson, Robson, and Marks, 1950) that mesenchymal 

 tissues in shielded areas may supply a factor that facilitates regeneration 

 of blood-forming tissue. It is of interest that spleen transplants (Jacob- 

 son, Simmons, Marks, and Eldredge, 1951; Jacobson, Simmons, Marks, 

 Gaston, et al., 1951) and spleen homogenates (Cole et al., 1952) facilitate 

 recovery and reduce radiation mortality in mice. Injection of lympho- 



