In 14 alcoholic patients, the degree of hepatic architectural destruction was graded (preserved architecture; nodules alternating with preserved architecture; totally destroyed architecture) and related to portal pressure. A positive correlation was found between the degree of architectural destruction and both wedged hepatic vein pressure (r = 0.72, p < 0.01) and wedged-to-free hepatic vein presure (r = 0.67, p < 0.02). Degree of fatty change, fibrosis, inflammation, necrosis and occurrence of Mallory bodies showed no correlation with portal pressure. After morphometrical evaluation of liver biopsies, no significant correlation was found between mean hepatocyte volume or relative sinusoidal vascular volume and portal pressure. To test whether an increase in hepatocyte volume compresses the vascular structures and causes portal hypertension, the ratio of relative sinusoidal vascular volume to mean hepatocyte volume, which expresses the compression of the vascular structures exerted by enlargement of hepatocytes, was related to portal pressure. No significant correlation was found. Further, mean hepatocyte volume was not significantly correlated to relative sinusoidal vascular volume. The present findings are in accordance with the hypothesis that elevated hepatic vascular resistance and portal pressure in alcoholic liver disease are in part detemined by the severity of the hepatic architectural destruction and subsequent distorsion and compression of the efferent vein system. Parenchymal changes, including changes in hepatocyte volume, seem to be of minor importance.