164 INTERNAL SECRETION 



it is not possible to produce chronic progressive suppression of 

 the suprarenal function experimentally and, by this means, acquire 

 a more intimate knowledge of the consecutive symptoms. 



Moreover, as the results of extirpation of the suprarenals do 

 not in any way resemble the clinical symptoms of Addison's 

 disease, our reference of the individual symptoms of the latter 

 condition to a suppression of the suprarenal function is, neces- 

 sarily, more or less hypothetical. 



What is known of the physiological activity of the internal 

 secretion of the adrenal system makes it easy to understand that 

 the reduction or suppression of the function of that system should 

 be followed by hypotonus, reduction in blood-pressure, and the 

 consecutive symptoms of cerebral anaemia. There was also at one 

 time a disposition to explain the adynamia the extreme 

 muscular weakness so characteristic of Addison's disease, which 

 has been demonstrated objectively by Langlois by means of 

 Mosso's ergograph by a lack of the tonic suprarenal secretion. 

 But a better acquaintance with the physiological effects of 

 adrenalin shows that there is no justification for ascribing to this 

 substance a controlling influence upon the tone of the striated 

 muscles. As we shall see later, adrenalin affects the sympathetic 

 nerve-endings only. The muscular asthenia of Addison's disease 

 is to be explained only by the most complicated hypotheses. The 

 most tenable theory is that, adrenalin being essential to the 

 metabolism of the carbohydrates, its reduction is attended by a 

 loss in the metabolism of glycogen, glycogen being essential to 

 the performance of muscular function. 



The asthenic symptoms and the gastro-intestinal disturbances 

 are by many authors attributed to the antitoxic activity of the- 

 suprarenal cortex. The sole symptom which invariably follows 

 suppression of the suprarenal function in both man and 

 animals, is emaciation. Up to the present, however, we have 

 no knowledge of the metabolic changes in animals to which 

 this emaciation is due. The information which we possess con- 

 cerning the metabolic changes in Addison's disease in man is of 

 too scanty a nature to supply -an answer to the problem. 



The origin of the pigmentation of the skin and mucous 

 membranes, the typical bronze skin (melanoderma) of Addison's 

 disease, is very difficult of explanation. Once again let it be 

 said that, up to the present, no one has succeeded in producing, 

 under experimental conditions free from objection, a pigmentation 

 of the skin in animals. The pigmentation of the skin is a fairly 

 constant, and frequently a very early, symptom in Addison's 

 disease. It first shows itself in the face and hands, then it affects 

 the neck and arms and, finally, spreads to the trunk and lower 

 extremities. The parts of the skin which are normally pigmented 

 are usually attacked first and acquire a deeper colour. The distri- 

 bution is affected by external conditions, such as exposure to 



