XXXX -induced @entity382 : pathogenesis and role in the production of portal @entity101 .

@entity1 @entity382 @entity82 @entity5881 @entity101 @entity167 @entity972
@entity382 after chronic @entity167 consumption results from an increase in cell size and not in cell number. About 50--60% of the increase in liver weight is accounted for by an increase in intracellular water, while extracellular water remains constant. Therefore, a substantial reduction in the ratio of extracellular to intracellular water occurs. Intracellular @entity972 can osmotically account for 40--50% of the excess water retained in the hepatocytes. It is proposed that an increase in hepatocyte size after chronic @entity167 consumption compresses vascular-sinusoidal pathways. This results, after a threshold in cell size is exceeded, in increased intrahepatic and portal pressure. Possible factors responsible for the threshold are proposed. By applying the concept that animal cells act as osmometers, a new in vitro model has been developed to study the relationship between cell enlargement and portal pressure. In this model, the existence of a threshold and the generation of portal @entity101 associated with hepatocyte enlargement have been demonstrated. In @entity1 with @entity5881 , a threshold in hepatocyte size enlargement (1600--1700 micrometer 2) before pressures were increased was also observed. In these @entity1 , a strong correlation was also found between hepatocyte size and intrahepatic pressure. The same correlation occurs regardless of the presence or absence of @entity82 , therefore suggesting that a major determinant of portal @entity101 in @entity82 is cell size and not the existence of nodules of fibrous septa. The higher portal pressures found in cirrhotics may be explained by the fact that these @entity1 have larger hepatocytes.
