1. Isolated perfused cirrhotic rat livers were used to study the effects of an increase in portal perfusion pressure and portal flow on the microcirculation and viability of the hepatocytes. Cirrhosis was induced by CCl4, and Krebs-Ringer bicarbonate buffer solution was used as the perfusate. Portal perfusion pressures were increased incrementally between 25 and 45 cm H2O. The viability of the livers was assessed and histological studies were performed under light and electron microscopy. 2. An increase in portal perfusion pressure induced an increase in hepatic flow in all the experiments (P < 0.05). Hepatic flow was 2.52 ml min-1g-1 of liver (SD 0.67; n = 5) at basal pressure compared with 4.19 ml min-1g-1 of liver (SD 0.93; n = 5) and 5.91 ml min-1g-1 of liver (SD 0.63; n = 5) when pressures were raised to 25 and 45 cmH2O, respectively. Portal perfusion pressure and hepatic flow were correlated (r = 0.908; P < 0.001; n = 30). 3. Production of the enzyme alanine aminotransferase (EC 2.6.1.2) increased significantly from 5.69i.u. ml-1min g-1 of liver (SD 3.62; n = 5) to 23.53i.u. ml-1min g-1 of liver (SD 16.7; n = 5) when the perfusion pressure was raised from baseline to 30 cmH2O. In all the cases the porto-caval gradient of enzyme production was within the normal range. No correlation existed between the release of enzyme and portal perfusion pressures.(ABSTRACT TRUNCATED AT 250 WORDS)