Abstract
The occlusion of portal branches to a portion of the rabbit's liver leads to a progressive and ultimately complete atrophy of the parenchyma in the region deprived of portal blood and to hypertrophy of the hepatic tissue elsewhere, which receives such blood in excess. Three fourths of the liver may thus be reduced to a fibrous tag within two months, while the remaining fourth attains the bulk of the entire original organ. The atrophy is simple, unaccompanied by obvious degenerative changes or by the least connective tissue replacement. More important, it is conditional in nature, failing to progress when the bile duct from the proliferating liver tissue is ligated and hypertrophy checked in this way.
Preliminary experiments indicate that these facts hold for the dog, though the changes go on more slowly in the canine liver. After three months the tissue deprived of portal blood has diminished to about one third of its original bulk. That such atrophy is conditional is proven by its relative failure to occur in the absence of a compensating parenchyma, as when the portal stream is completely diverted from the whole liver by way of an Eck fistula.
The bile secreted from a portion of the rabbit's liver far advanced in an atrophy of the sort described, and competing with a large liver mass which received the entire portal stream, is almost colorless and may give but a weak Pettenkofer reaction. Glycogen, though, is present in the atrophic cells in approximately the same amount and distribution as in the hypertrophic parenchyma of the same animal.
The type of local liver destruction here considered, which is dependent upon hypertrophy elsewhere, contrasts interestingly with the local hypertrophy dependent upon destruction which has long been familiar to pathologists.
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