PATHOLOGY: PEARCE AND BROWN 
463 
maffin content of the adrenals while others, such as sodium cacodylate, 
salvarsan, and neosalvarsan, cause a rapid and marked decrease in this 
substance, as judged by the color of the medullary cells after fixation 
in Miiller's fluid. 
From these observations it appears that the adrenotropic action of 
arsenicals is one of the most constant and important features of arsenical 
intoxication and we suggest that therapeutic doses of some arsenicals 
may be found to produce definite stimulation of the adrenal glands. 
VARIATIONS IN THE CHARACTER AND DISTRIBUTION OF 
THE RENAL LESIONS PRODUCED BY COMPOUNDS 
OF ARSENIC 
By Louise Pearce and Wade H. Brown 
ROCKEFELLER INSTITUTE FOR MEDICAL RESEARCH. NEW YORK 
Presented to the Academy. July 3. 1915 
The chemical agents employed in the production of experimental 
nephritis are usually divided into two classes, those producing tubular 
lesions and those producing vascular lesions, to the latter group of 
which the compounds of arsenic have been assigned. From a study of 
the renal lesions produced by a large number of arsenicals, however, we 
have been led to question the validity of such a classification and to view 
the pathogenic action of such substances from the standpoint of their 
chemical constitution as well as their arsenic content. 
The classical hemorrhagic kidney of arsenious acid is by no means 
constant for all compounds of arsenic. Grossly, the kidneys of dogs 
given lethal doses of such substances as arsenious acid, salvarsan, neo- 
salvarsan, galyl, arsenophenylglycine, atoxyl, and arsacetin are separ- 
able into two extreme groups, the red and the pale kidneys, with tran- 
sitional types in which the predominating changes ally them more closely 
with the one group or the other. In the group of red kidneys, conges- 
tion and hemorrhage are the dominant features of the arsenical action, 
while in the pale kidneys, the dominant lesion is tubular. 
Upon closer analysis of the gross and microscopic changes we can make 
a further differentiation of the action of compounds that produce kid- 
neys of the one or the other of these types. For example, arsenious 
acid, salvarsan, neosalvarsan, and galyl all produce red kidneys, but the 
congestion and hemorrhage produced by arsenious acid is diffuse in 
character with but slight tubular necrosis, while the vascular injury 
of salvarsan, neosalvarsan, and galyl is more pronounced in the cortex 
and the boundary zone and is accompanied by much more marked 
