166 G. K STEWART 



When this f)oint has been reached it must be assumed that further forma- 

 tion in the denervated gland practically ceases, since if there is any "spill" 

 into the blood when the epinephrin-secretory nerves are eliminated it is so 

 small as to escape detection, in some cases even by rabbit intestine seg- 

 ments, which would have been capable of responding to concentrations of 

 epinephrin corresponding to one one-thousandth of the ordinary output. 



There is nothing in this inconsistent with the view that although a 

 deficiency in the store itself constitutes a "stimulus" to new formation of 

 epinephrin till the saturation point has been reached, a "quick-charging" 

 nervous mechanism exists which hastens epinephrin formation, and that 

 when the liberation of epinephrin is accelerated through excitation of the 

 nervous system, the auxiliary mechanism which speeds up the formation 

 of epinephrin is normally excited at the same time. In animals dead of 

 infections of various kinds, the suprarenal protected by section of its 

 nerves has been seen to have a markedly greater store of epinephrin than 

 its fellow, but this is not true of all infections. In man'Comessatti(&) ob- 

 tained very variable results in an investigation of the epinephrin store in 

 70 patients dead of various diseases, including chronic nephritis. As he 

 justly remarks, such observations have a very limited value. Lucksch(t?) 

 found that in animals poisoned with diphtheria toxin, the epinephrin dis- 

 appeared altogether or in great part from the suprarenals, as shown by the 

 great diminution in the presscr effect of extracts (cf. Tscheboksaroff(&), 

 1911). Ritchie and Bruce confirmed this, showing that in guinea pigs 

 affected by diphtheria toxemia running a slow course the suprarenal 

 medulla is devoid of epinephrin, whereas in hyperacute infection death 

 occurs before the depletion becomes total. Schmorl and Ingier, however, 

 saw no diminution in the epinephrin content of the suprarenals in man in 

 the majority of cases of acute infection, especially diphtheria. They 

 employed the colorimetric method of Comessatti. 



That little or no epinephrin should be found in the suprarenals in 

 Addison's disease (Oliver and Schafer, Ingier and Schmorl et al.) has no 

 special pathological significance. A diseased suprarenal is very likely to 

 lose its epinephrin store. The edema of the suprarenal which is apt to 

 result from trauma in its immediate vicinity, especially in the rabbit, is 

 associated with great diminution in the epinephrin store, which is regained 

 after a time when the edema has subsided (Stewart and Rogoff(c), 1916). 

 Cramer ( c) has described histological changes in the suprarenal medulla 

 under the influence of severe cold and other conditions. Some observers 

 have endeavored to show an interrelation between the suprarenal medulla 

 and other endocrine tissues by determining whether changes occur in the 

 amount of the epinephrin store in various experimental conditions. Thus, 

 Herring(a.) (b) stated that thyroid feeding caused an increase and thy- 

 roidectomy a decrease in the epinephrin store. For the reason already 

 mentioned, this would have no direct bearing upon what is after all the 



