The effect of hepatic artery inflow on regeneration, hypertrophy, and portal pressure of the liver following 50 per cent hepatectomy in the dog.

Abstract

Abstract Interruption of the hepatic arterial supply in the dog followed by hemihepatectomy has no deleterious effect on the subsequent regeneration or function of the remaining liver. Deprivation of portal flow to half of an intact liver will result in atrophy of that portion and compensatory hypertrophy of the remaining half. This hypertrophy is unaffected by loss of arterial inflow. Thus hepatic arterial inflow appears to be inessential for either regeneration or hypertrophy of the normal canine liver. Hepatic artery ligation significantly decreases the portal hypertension resulting from hemihepatectomy or ligation of a portion of the portal vein, yet subsequent regeneration and hypertrophy are unaffected. Thus increased intrasinusoidal pressure is probably not a controlling factor in regeneration or hypertrophy of the normal canine liver. The above data may apply to the normal human liver: however, in states where compensatory increase of portal blood-flow cannot occur, hypoxic liver failure may result from interruption of hepatic arterial inflow.