The occlusion of portal branches to a part of the liver of the rabbit leads to a progressive and ultimately complete atrophy of the parenchyma in the region deprived of portal blood, and to hypertrophy of the rest of the hepatic tissue which receives such blood in excess. Three-fourths of the liver may thus be reduced to a fibrous tag within 2 months, while the remaining fourth attains the bulk of the entire original organ. The atrophy is simple, unaccompanied by obvious degenerative changes or by any connective tissue replacement. More important, it is conditional in nature, failing to progress when the bile duct from the proliferating tissue is ligated and its hypertrophy checked in this way.
There are indications in the literature that an atrophy conditional on hypertrophy, such as is here described, occurs in man after local portal occlusion. And some experiments in our laboratory, not yet completed, show definitely its occurrence in the dog. The changes take place slowly in the canine liver. After 3 months the tissue deprived of portal blood has diminished to about one-third of its original bulk. The conditional character of the atrophy is proven by its failure to occur to any similar degree in the absence of a compensating parenchyma, as when the portal stream is diverted from the whole liver by way of an Eck fistula.
Is the atrophy functional? If so, its completeness would indicate that the liver has no essential activity—none on which its maintenance depends—that it is not intimately connected with substances derived from organs drained by the portal system. Observations on the rate of hypertrophy after local diversion of the portal stream and on the character of the bile secreted by the atrophic tissue may be taken to favor such a view. The hypertrophy is nearly, perhaps quite, as rapid as if the tissue deprived of portal blood had been removed from the body. The bile secreted from a liver mass far advanced in atrophy and competing with a large bulk of parenchyma that receives the entire portal stream is almost colorless and may give but a weak Pettenkofer reaction. Glycogen, on the other hand, is present in the atrophic cells in approximately the same amount and distribution as in the hypertrophic liver tissue of the same animal.
The fact that a parenchymal shift follows local disturbances in the portal stream has a bearing on the cause of certain alterations in the shape of the normal liver that have been loosely attributed heretofore to pressure from the surrounding organs. It also has some interest in connection with pathological changes. Liver hypertrophy dependent on a preceding destruction has long been known to pathologists. Now a type of destruction dependent on compensatory hypertrophy must also be reckoned with. The occurrence of changes of the latter character will explain certain of the lesions observed in diseases that involve a disturbance of the portal flow to portions of the liver substance.