The bile ducts from three-quarters of the liver substance in dogs and monkeys can be obstructed without any clinical evidence developing of pigment or cholate accumulation in the organism. And in the dog nineteen-twentieths of the liver substance can be placed in stasis without the occurrence of tissue icterus such as regularly follows total obstruction in this animal. There is no reason to suppose that this will not be found true in the monkey as well. Always a local obstruction results sooner or later in atrophy of the affected tissue with compensatory hypertrophy elsewhere. Thus as time passes the derangement of function produced by the sudden stasis is progressively lessened.
The plasma of the dog and monkey, unlike that of man, is normally free from bilirubin, and this pigment so readily escapes from the blood into the urine that bilirubinuria is often to be found in the dog in the absence of bilirubinemia, while the latter is never met with alone in either animal. It follows that in both species the renal threshold for bilirubin is much lower than in man,—if indeed one can be said to exist at all.
The amount of biliary obstruction required to produce jaundice in human beings is probably as great as in the experimental animals with which we have dealt. The clinical jaundice encountered in association with local liver lesions should be viewed not as the result of local bile resorption, but as due to a general injury to the hepatic parenchyma or ducts, or to blood destruction.