On the characteristics of alcohol-induced liver enlargement and its possible hemodynamic consequences

Abstract

Chronic consumption of alcohol leads to an increase in liver weight, primarily due to an increase in hepatocyte volume. About 50–60% of such an increase is due to an increase in intracellular water. Accumulation of intracellular K + osmotically accounts for about one half of the increase in intracellular water, while an increase in soluble proteins plays only a minor role in such an increase in cell volume. The increase in intracellular water is accompanied by a relative reduction in water in the extracellular space, probably due to compression of the extracellular volume by the enlarged hepatocytes. It is suggested that such an increase in hepatocyte size, with an attending reduction of the extracellular volume, results in an increased resistance to blood flow through the liver and thus in an increase in portal pressure. In alcoholics, portal and intrahepatic pressure correlate with cell size both in cirrhotics (r=0.79) and in non-cirrhotics (r=0.74), thus suggesting that cell enlargement plays a major role in the production of portal hypertension in the alcoholic.