268 



H. HAGER, W. HIRSCHBERGER AND A. BREIT 



PMN 



AR 



^^^■■■^^m^,^ 



•V^^" 

 f^-^-" 



^ 



<: -0 '-'- ■ ■ ^ ^-^ 'fl^^ 





0*. ■*» 







/^: 



.-^Z 



..s.^' 





,M 



EF 



.i 



Fig. 8. Cerebral cortex, 73 hr survival after exposure to 45,000 r, showing a rela- 

 tively well preserved small artery (Ar) surrounded by macrophages (M) and poly- 

 morphonuclear leucocyte (PMN) in an area of extensive necrosis. EF, ingested ery- 

 throcyte fragments. X 4,000. 



membranes and occasional mitochondria are still recognizable. Erythrocytes 

 and macrophages are seen swimming free in the severely damaged tissue. 



Figure 10 is a high magnification of a siinilar region to show the variety 

 of intracytoplasmic inclusions in macrophages. The significance and origin 

 of similar products of decomposition in cerebral necrosis following me- 

 chanical trauma has already been reported. fHager, 1960). In the same 

 figure, the persistent preservation of membranous components of the neuropil 

 is evident. Figure 1 1 shows a nerve cell also in a severe stage of destruction. 

 Nuclear and cytoplasmic membranes are interrupted. The internal arrange- 

 ment of the mitochondria is broken down, and the normal fine structural 

 organization of the cytoplasm is greatly altered. The nucleoplasm is vacu- 

 olated, no longer fills the nuclear envelopes, and is obviously abnormal, 

 though the appearance differs greatly from the shrunken pyknotic nuclei of 

 the granular cells of the cerebellum. Capillaries from areas of total necrosis. 



