HYPOADRENTA 315 



sympathetic irritability, i. e., that epinephrin is of importance in the 

 metabolism of the sympathetic nervous system, particularly of the myo- 

 neural "receptive substance." Hoskins and Wheelon(&), however, were 

 unable to find any evidence to show that the sympathetic system suffered 

 primarily in any degree from suprarenal extirpation. There is no satis- 

 factory evidence of an experimental nature for the belief that epinephrin 

 deficiency is the cause of death following extirpation. It seems probable 

 that death is due to a loss of the cortical, rather than the chromaphil tissue 

 of the gland. 



Destructive lesions of the glands have frequently been experimentally 

 produced by the injection of various toxins, either bacterial (diphtheria, 

 tetanus, pneumococcus, streptococcus, etc.) or chemical (arsenic, mercury, 

 lead, etc.). The first result of such injections is usually the production of 

 hyperemia of the gland, which some authors regard as indicating a state of 

 hyperfunction. If the intoxication is severe, however, an arrested func- 

 tion of the gland results, due to the destructive lesions produced (hemor- 

 rhage, softening or necrosis), with the clinical symptoms of hypofunction. 

 Schur and Wiesel(fr) have observed that prolonged narcosis with chloro- 

 form, or ether, in rabbits, may cause the disappearance of the chromaphil 

 substance of the medulla, followed by a rapid return to a normal content in 

 a few hours. Graham was able to produce necrotic lesions in the cortex 

 by chloroform, dichlormethane, and tetrachlormethane, inhalations in 

 animals; also less extensive lesions by the subcutaneous injection of phenol. 

 His observations led him to believe that the suprarenal cortex is very sensi- 

 tive to poisons, and its cells readily injured or destroyed by these, and fur- 

 ther that the cortical parenchyma possesses a power of regeneration, when 

 the lesion is removed. Lattes(fr) has adduced some experimental evidence 

 in support of the view that superficial burns may cause death by inducing 

 suprarenal deficiency. He found that in animals killed 5-7 days after the 

 infliction of a burn, the cortex showed characteristic changes, consisting 

 of hyperemia, accompanied by hemorrhages. The lipoids of the cortex 

 were considerably diminished and the cholesterol esters almost entirely 

 absent, A study of the epinephrin content of the gland, following acute 

 intoxications experimentally produced in dogs, has been made by Syden- 

 stricker, Delatour and Whipple. In this condition they found a low epi- 

 nephrin index in the glands. After recovery from a sublethal dose it was 

 observed that a rapid rise to a point considerably above the normal might 

 occur. Certain liver poisons, as chloroform, phosphorus and hydrazin, 

 were found to cause a drop in the index to about half the normal. 



A classification of the various types of suprarenal deficiency has been 

 attempted by clinicians. The French writers, mainly, have recognized 

 three forms, the acute, the subacute, and the chronic. The acute form 

 is characterized by the severity of the symptoms, and is usually associated 

 with extensive destructive lesions in the gland, terminating fatally, as a 



