Hepatic blood flow (EHBF) was measured by the clearance-and-extraction method using indocyanine green (ICG) in 15 patients hospitalized with acute viral hepatitis. In 10, the single injection technique (corrected for hepatic extraction and mean splanchnic circulation time, colloidal denatured human serum albumin-labeled with radioiodine, CA131I) was employed simultaneously to estimate flow (CABF).Despite considerable clinical diversity (plasma bilirubin ranging, for example, from 2.4 to 32.0 mg%), EHBF fell within normal limits (930 to 2,130 ml per min) in all but two patients (A.V., 890 ml per min and C.G., 2,430 ml per min), and was in good agreement with CABF. Although hepatic extraction of sulfobromophthalein was so greatly reduced (less than 10%) that it could not be employed for estimating EHBF, both ICG and CA131I extractions were well maintained (21 to 73%, normal 63%, and 50 to 76%, normal 95%, respectively). Extraction of ICG returned to normal levels as jaundice cleared whereas CA131I extraction remained depressed indicating improvement in hepatocellular function without redistribution of blood flow within the liver during recovery.Since the liver was obviously enlarged in all patients and since measurements of circulating splanchnic blood volume by the regional dilution method fell below the normal mean in eight of 10 patients, it was inferred that hepatomegaly was a result of augmented cell mass rather than vascular engorgement and that hepatic blood flow decreased relative to tissue volume. Splanchnic oxygen arteriovenous difference and oxygen uptake also fell within normal limits in five patients suggesting that the increment in liver mass might be ascribed chiefly to cellular hydration.Normal values for wedged hepatic venous pressure (10 patients) indicated that postsinusoidal resistance remained unaltered and that cellular swelling did not affect postsinusoidal resistance or perfusion. The observation reported by other workers that portal venous pressure may increase during the course of acute viral hepatitis must, therefore, be attributed to an increase in pre-sinusoidal portal venular resistance. It was concluded that inflammatory infiltration and increased capillary permeability within the portal tracts may contribute to the disease process by interfering both with portal venous inflow and biliary outflow.