In the present study we have characterized the evolution of changes in syst
emic haemodynamics (thermodilution in conscious animals) and sodium balance
(metabolic cages) in a model of liver cirrhosis induced by chronic bile du
ct ligation (BDL). Mean arterial pressure (BDL, 111.5 +/- 4.7 mmHg; sham-op
erated, 122.9 +/- 3.0 mm Hg) and peripheral vascular resistance (BDL, 2.63/-0.08 units; sham-operated, 2.93+/-0.09 units) were lower in BDL rats from
day 12 after surgery and decreased progressively throughout the following
days. Portal hypertension was evident earlier in BDL rats and was maintaine
d throughout the study period. Cardiac index (BDL, 58.8+/-3.9 ml . min(-1)
. 100 g(-1); sham-operated, 43.9+/-1.5 ml . min(-1) . 100 g(-1)) and stroke
volume (BDL, 147.2 +/-12.7 ml . beat(-1) . 100 g(-1); sham-operated, 109.0
+/-4.2 ml . beat(-1) . 100 g(-1)) were significantly elevated in the BDL ra
ts only from day 18 after surgery. There were no significant differences in
sodium balance between the groups until day 16 after surgery, at which tim
e BDL animals started to retain significantly more sodium than the controls
. Sodium retention increased progressively, and at day 20 BDL rats had reta
ined 0.7 mmol/100 g more than the control animals (accumulated retention: B
DL, 2.2+/-0.2 mmol/100 g; sham-operated 1.5+/-0.2 mmol/100 g). Plasma renin
activity and aldosterone concentration were not elevated in the BDL animal
s at days 12, 16 or 20 after surgery. These data indicate that the BDL rat
model shows early portal hypertension, peripheral vasodilation and arterial
hypotension, several days before sodium retention is detectable, and in th
e absence of changes in plasma levels of renin and aldosterone. Overall, th
ese data suggest that, in the BDL rat model, sodium retention is secondary
to portal hypertension and peripheral vasodilation.