Haemodynamic and renal evolution of the bile duct-ligated rat

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.