title: Haemodynamic and renal evolution of the bile duct-ligated rat.
abstract: In the present study we have characterized the evolution of changes in systemic haemodynamics (thermodilution in conscious animals) and sodium balance (metabolic cages) in a model of liver cirrhosis induced by chronic bile duct ligation (BDL). Mean arterial pressure (BDL, 111.5+/-4.7 mmHg; sham-operated, 122.9+/-3.0 mmHg) 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 maintained 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 rats only from day 18 after surgery. There were no significant differences in sodium balance between the groups until day 16 after surgery, at which time BDL animals started to retain significantly more sodium than the controls. Sodium retention increased progressively, and at day 20 BDL rats had retained 0.7 mmol/100 g more than the control animals (accumulated retention: BDL, 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 animals 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 the absence of changes in plasma levels of renin and aldosterone. Overall, these data suggest that, in the BDL rat model, sodium retention is secondary to portal hypertension and peripheral vasodilation.
authors.affiliation: Unidad de Aparato Digestivo, Hospital de la Vega Baja, Orihuela, Alicante, Spain.
authors.forename: C
authors.initials: C
authors.lastname: Martínez-Prieto
authors.forename: M C
authors.initials: MC
authors.lastname: Ortíz
authors.forename: L A
authors.initials: LA
authors.lastname: Fortepiani
authors.forename: J
authors.initials: J
authors.lastname: Ruiz-Maciá
authors.forename: N M
authors.initials: NM
authors.lastname: Atucha
authors.forename: J
authors.initials: J
authors.lastname: García-Estañ
mesh_terms: D000450:Aldosterone / Q000097:blood; D000818:Animals; D001652:Bile Ducts; D004195:Disease Models, Animal; D004231:Diuresis / Q000502:physiology; D006128:Growth / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology*; D006975:Hypertension, Portal / Q000209:etiology; D008026:Ligation; D008106:Liver Cirrhosis, Experimental / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D008297:Male; D009318:Natriuresis / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000097:blood; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D000450:Aldosterone; D012083:Renin