THE PATHOLOGY OF AZOTURIA. 
177 
prolonged rest; and parallel with this prolongation of rest and 
decline of albumen, the susceptibility of the horse to azotu- 
ria retrogrades and finally ceases. 
This hyperalbuminosis is accepted by some as the one 
essential factor in the production of the disease, but this doc¬ 
trine is opposed by the clinical fact that this absolute plethora 
may and does exist, without in any case producing the disease 
except in conjunction with muscular exertion. 
Consequently, while accepting the theory of hyperalbumi¬ 
nosis as the first essential factor in the causation of azoturia, 
there yet remain for explanation other phenomena in the 
clinical history of the disease and we are led to inquire why 
muscular exertion is necessary in the development of the 
pathological condition, and what changes are produced in the 
animal economy, especially in the blood, by this sudden exer¬ 
tion. 
Those pathologists relying wholly upon the theory of 
hyperalbuminosis to explain all the phenomena, resort to 
various means. Thus Prof. Williams suggests the rapid oxi¬ 
dation of albuminoids upon exertion, with a resultant sur¬ 
charging of the blood with uric, hippuric acid, &c., yet he 
fails to explain why animals sparingly exercised and doubtless 
as truly hyperalbuminotic as any, yet do not contract azoturia 
when suddenly put to severe exertion. 
Dieckerhoff claims the development, through the agency 
of muscular effort, of a toxic ferment which pre-exists in the 
blood, but the careful observer must admit that, up to the 
moment of attack, the subject bears every possible evidence 
of typical health. That prompt quietude in the early stages 
of the disease affords equally prompt relief, while, were a 
toxic ferment present it would not cease to act with cessation 
of exercise ; and moreover, muscular exertion would not likely 
be essential to its awakening and development; and further, 
careful light exercise for a few hours prior to hard labor con¬ 
stitutes an invincible guard against the disease, about the 
animals subject to it, although such light preliminary exertion 
could by no know means destroy an existing toxic ferment. 
In searching for the remaining essential factors in the 
