TOXINS AND INFECTIONS 265 



jury and the dosage employed. With chloroform narcosis, 237 

 an immediate damage is produced which is rapidly repaired. 

 The earliest changes observed are congestion of the medulla 

 and inner cortical zones followed by degeneration of the cells 

 of the zona reticularis. A large proportion of the cortical cells 

 may be ultimately destroyed. Recovery sets in within 48 

 hours during which the undamaged cells in the more peripheral 

 layers of the cortex show active mitosis. This regenerative 

 process is similar to that observed following necroses due to 

 infectious processes. The regenerative capacity of the adrenal 

 is entirely comparable in its extent with that of other organs 

 as, for example, the liver. The zona glomerulosa and the outer 

 portion of the fasciculata constitute the growth center where 

 regeneration occurs, the newly formed cells being displaced in- 

 wardly to supply the loss at the inner layers. 



In contrast to the effects of chloroform inhalations, the in- 

 jection of diphtheria toxin produces a progressive injury of the 

 adrenals the repair of which is slow. 301 Large doses of the 

 toxin produce hemorrhages and focal necroses (chiefly in the 

 reticularis) which during repair are replaced in part by con- 

 nective tissue. Small doses decrease the lipid content (as ob- 

 served microscopically) of the cortex and cause widening of 

 the reticular zone at the expense of the fasiculata. Diphtheria 

 toxin also causes a marked reduction in the epinephrine con- 

 tent of the adrenals but this decrease, as Edmunds and John- 

 son 172 showed, is not the cause of the circulatory collapse ob- 

 served in the terminal stages of animals poisoned by this toxin. 



In scurvy and other diseases of inanition there is a marked 

 increase in the lipid content of the cortical cells with granula- 

 tion of the mitochondria. Administration of vitamin C to 

 scorbutic animals causes active regeneration of the injured 

 tissue. 301 



From observations in a number of diverse diseases, Elliott 181 

 showed that the storage and disappearance of the cortical lipid 

 occurred under conditions entirely different from those control- 



