THE ADRENALS AND ADDISON'S DISEASE 019 



of its nonprotein nature, epinephrine does not cause the j)ro(luction of 

 antibodies.''" 



Many studies have been directed to determine the relation of the 

 adrenal to hypertroi)hy of the heart and to interstitial nephritis with 

 high blood pressure. Some have found more or less increase in size in 

 the adrenals under these conditions, chiefly involving the cortex, 

 and a slight increase in the epinephrine content has been reported, 

 but it is very doubtful if these observations are of significance. ''' It 

 has been reported by several investigators that the blood in sucli condi- 

 tions contains sufficient epinephrine to permit of its detection and 

 measurement by its physiological effects (dilatation of the frog's iris, 

 contraction of the rabbit uterus or blood vessels, inhibition of con- 

 traction of the intestine). The critique of this work by Stewart, ^- 

 however, makes it necessary to discount most of the published results, 

 as being inadequately controlled. He found no epinephrine even in 

 blood coming direct from the adrenal veins, unless the gland had been 

 stimulated or manipulated, and none could be detected in the serum 

 from several patients with high pressure from various causes, as well 

 as in mental disturbances and exophthalmic goiter. Vaso-constrictor 

 substances may be present in serum, both normal and pathological, 

 wliich are not epinephrine. His negative results are corroborated by 

 Janeway and Park.'^^ Broking and Trendelenburg, '"'using a perfusion 

 method which they believe to be reliable, found a normal pressor effect 

 from the blood of persons with arteriosclerosis and high blood pressure, 

 a decrease in nephritis with high pressure, a great increase in exophthal- 

 mic goiter, and no changes in pregnancy, chlorosis and diabetes. 



Arterial Degeneration from Epinephrine." — An interesting result of repeated 

 injections of epineprhine into animals is the appearance of a marked atheromatous 

 degeneration of the aorta, with calcification. This was first observed by Josu6, 

 and since confirmed by Erb, Fischer, Gouget, Loeb and Githens, and many others. 

 These lesions are quite different from those of human aortic arteriosclerosis, the 

 chief change being degeneration of the muscle-cells of the media, without any con- 

 siderable inflammatory reaction. There is, however, more resemblance to the 

 atheromatous changes seen in the arteries of the extremities. They do not seem 

 to be due to the heightened blood pressure, since simultaneous administration of 

 substances that keep the blood pressure down does not prevent the atheroma from 

 developing (Braun), while other substances that raise blood pressure, such as 

 nicotine (Josuc) or pyrocatechin (Loeb and Githens), do not cause atheroma. Pre- 

 sumably, therefore, epinephrine causes the arterial changes by a direct toxic 

 action, but the influence of increased blood pressure cannot be entirely excluded. 

 However, slow injection of epinei)hrine, so regulated that there is an increase in 

 the blood content without significant rise of pressure, fails to produce arterio- 

 sclerosis.''^ Myocardial degeneration is also observed in experunental animals, 



7" See Elliott and Durham, Jour, of Physiol., 1906 (34), 430. 



"' See Pearce, Jour. Exper. Med., 190S (10), 735; Thomas, Ziegler's Beitr., 

 1910 (49), 228. 



'■' Jour. Exp. Med., 1911 (14), 377; 1912 (15), 547; also Rogoff, Jour. Lab. 

 Clin. Med., 1918 (3), 209. 



" Jour. Exp. Med., 1912 (16), 541. 



'^Deut. Arcli. klin. Med., 1911 (103), 168. 



" Literature given by Saltykow, Cent. f. Path., 1908 (19), 369. 



'^ van Leersum and Rassers, Zeit. exp. path., 1914 (16), 230. 



