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In cirrhotic livers, the intrahepatic resistance is increased and drug elimination and portal transhepatic flow are decreased. The aim of our work was to study the effect of a twofold increase in portal blood flow during 2 hr on the hemodynamic parameters, drug elimination and hepatic viability in eight isolated perfused human cirrhotic livers. Using an oxygenated recirculating system with independent arterial and portal flows, we perfused livers with Kreb's buffer bicarbonate solution, bovine serum albumin (20 gm.L-1) and human red blood cells (hematocrit 20%). The flow was maintained at a basal level of 0.713 +/- 0.19 L/min for 1 hr and then increased and maintained for 2 hr at twice the basal flow. Portal pressure-portal flow curve slopes were linear (27.04 +/- 21.06 mm Hg.L-1 x min; range = 6.43 to 60.8) and correlated with intrahepatic resistance during the basal-flow period (r = 0.87, p < 0.01). Parameters registered during the basal- and high-flow periods were compared by use of Student's t test: portal pressure increased from 23.5 +/- 7 to 37.3 +/- 16.7 mm Hg (p < 0.05); arterial pressure increased from 80.3 +/- 19 to 103.5 +/- 26 mm Hg (p < 0.005); hepatic artery flow resistance increased 31.9% (from 690.1 +/- 218 to 899.4 +/- 269 mm Hg.L-1 x min; p < 0.005); indocyanine green clearance increased by 28.2% (from 86.0 +/- 58.3 to 109.2 +/- 74.8 ml.min-1 x kg liver-1; p < 0.04). No significant differences were observed in enzyme release, biliary flow (n = 5) and oxygen consumption. Histological examinations demonstrated sinusoidal dilatations in six of eight cases.(ABSTRACT TRUNCATED AT 250 WORDS)

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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)