Serial natriuretic response to atrial peptide in preascitic bile duct ligated dogs

1990 ◽  
Vol 68 (11) ◽  
pp. 1396-1400 ◽  
Author(s):  
Elizabeth Maher ◽  
Peter Cernacek ◽  
Mortimer Levy
Keyword(s):  
Bile Duct ◽  
Sodium Excretion ◽  
Bile Duct Ligation ◽  
Control Period ◽  
Sodium Balance ◽  
Sodium Retention ◽  
Time Intervals ◽  
Similar Time ◽  
Duct Ligation ◽  
Time Periods

We determined if nine precirrhotic unanaesthetized dogs with chronic bile duct ligation (CBDL) responded uniformly to atrial natriuretic peptide (ANF) by infusing this peptide sequentially over 8–12 weeks at 175 ng∙kg−1∙min−1 and observing the natriuretic response. ANF was administered every 2 weeks post-CBDL until the 8th week and given again during the cirrhotic phase with ascites present (10–12 weeks post-CBDL). Sodium balance studies were conducted at similar time intervals. During the control period and at weeks, 2, 6, and 8 post-CBDL all dogs responded to ANF with a significant change in sodium excretion (ΔUNaV, 50–240 μequiv./min). At these times, all dogs were in sodium balance. At week 4 and during the ascitic period, heterogeneity of response to ANF was observed. In the former interval, five dogs responded (ΔUNaV, 75–230 μequiv./min) and four did not, while in the latter interval, five dogs responded (ΔUNaV, 50–240 μequiv./min) and three did not (one dog died). In both time periods, there was severe urinary sodium retention (daily UNaV, 11 ± 3 and 2 ± 1 mequiv./day, respectively) while the dogs were ingesting 45 mequiv. Na+/day. The heterogeneity of natriuretic response was not correlated to plasma immunoreactive ANF, renin, or aldosterone levels. Plasma volume was significantly expanded from control during both intervals. We conclude that there is transient sodium retention during the 4th week post-CBDL, and that this period is associated with the heterogeneity of natriuretic response to ANF, despite the absence of ascites or edema.Key words: sodium excretion, cirrhosis, edema.

Pathogenesis of Salt Retention in Dogs with Chronic Bile-Duct Ligation

1982 ◽  
Vol 62 (1) ◽  
pp. 65-70 ◽  
Author(s):  
C. Chaimovitz ◽  
U. Alon ◽  
O. S. Better
Keyword(s):  
Bile Duct ◽  
Sodium Excretion ◽  
Control Period ◽  
Extracellular Volume ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Sodium Retention ◽  
Plasma Aldosterone Concentration ◽  
Duct Ligation

1. The present study investigates the role of mineralocorticoids in the pathogenesis of salt retention and ascites in dogs with chronic ligation of the common bile duct (CBDL). 2. After CBDL the natriuretic response to an intravenous sodium load [0.9% sodium chloride solution (150 mmol/l): saline; 10% of body weight] was markedly depressed. Urinary sodium excretion was 285 ± 62 vs 960 ± 58 μmol/min in the control period before CBDL (P < 0.001). This antinatriuresis was associated with a significant rise in plasma aldosterone concentration, from 52.5 ± 5.5 pg/ml before CBDL to 177 ± 50 pg/ml after CBDL (P < 0.02). Ascites was present in all salt-retaining CBDL dogs. 3. Bilateral adrenalectomy resulted in disappearance of ascites and in a rise in the natriuretic response to extracellular volume expansion. Urinary sodium excretion was 770 ± 124 μmol/min, a value significantly higher than in the CBDL dogs with intact adrenals (P < 0.001). Sodium balance studies in the adrenalectomized CBDL dogs during chronic deoxycorticosterone acetate (DOCA) treatment (25 mg/day) showed that in these animals there was failure to escape from the mineralocorticoid-induced sodium retention. Glomerular filtration rate and renal plasma flow did not change during the studies. 4. The present evidence supports the thesis that sodium retention in the CBDL dog results from a dual mechanism: (a) excess of circulating aldosterone and (b) an extra-adrenal factor which prevents escape from the salt-retaining effect of mineralocorticoids, in the CBDL dogs, thereby perpetuating the antinatriuresis in these animals.

Effects of chronic L-NAME on nitrotyrosine expression and renal vascular reactivity in rats with chronic bile-duct ligation

2008 ◽  
Vol 115 (2) ◽  
pp. 57-68 ◽  
Author(s):  
Antonia Alcaraz ◽  
David Hernández ◽  
David Iyú ◽  
Rubén Mota ◽  
Noemí M. Atucha ◽  
...  
Keyword(s):  
Bile Duct ◽  
Vascular Reactivity ◽  
Bile Duct Ligation ◽  
Sodium Balance ◽  
Biliary Cirrhosis ◽  
Sodium Retention ◽  
Vascular Response ◽  
Experimental Cirrhosis ◽  
Duct Ligation ◽  
Renal Vascular

In liver cirrhosis, elevated levels of NO and ROS (reactive oxygen species) might greatly favour the generation of peroxynitrite. Peroxynitrite is a highly reactive oxidant and it can potentially alter the vascular reactivity and the function of different organs. In the present study, we evaluated whether peroxynitrite levels are related to the progression of renal vascular and excretory dysfunction during experimental cirrhosis induced by chronic BDL (bile-duct ligation) in rats. Experiments were performed at 7, 15 and 21 days after BDL in rats and in rats 21 days post-BDL chronically treated with L-NAME (NG-nitro-L-arginine methyl ester). Sodium balance, BP (blood pressure), basal RPP (renal perfusion pressure) and the renal vascular response to PHE (phenylephrine) and ACh (acetylcholine) in isolated perfused kidneys were measured. NO levels were calculated as 24-h urinary excretion of nitrites, ROS as TBARS (thiobarbituric acid-reacting substances), and peroxynitrite formation as the renal expression of nitrotyrosine. BDL rats had progressive sodium retention, and decreased BP, RPP and renal vascular responses to PHE and ACh in the time following BDL. They also had increasing levels of NO and ROS, and renal nitrotyrosine accumulation, especially in the medulla. All of these changes were either prevented or significantly decreased by chronic L-NAME administration. In conclusion, these results suggest that the increasing levels of peroxynitrite might contribute to the altered renal vascular response and sodium retention in the development of the experimental biliary cirrhosis. Moreover, the beneficial effects of decreasing NO synthesis are, at least in part, mediated by anti-peroxinitrite-related effects.

Haemodynamic and renal evolution of the bile duct-ligated rat

2000 ◽  
Vol 98 (5) ◽  
pp. 611-617 ◽  
Author(s):  
Concepción MARTÍNEZ-PRIETO ◽  
M. Clara ORTÍZ ◽  
Lourdes A. FORTEPIANI ◽  
Jose Antonio RUIZ-MACIÁ ◽  
Noemí M. ATUCHA ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Bile Duct ◽  
Rat Model ◽  
Bile Duct Ligation ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Sodium Retention ◽  
Peripheral Vasodilation ◽  
Duct Ligation ◽  
Conscious Animals

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.

Haemodynamic Studies in Dogs with Chronic Bile-Duct Ligation

1976 ◽  
Vol 50 (6) ◽  
pp. 533-537 ◽  
Author(s):  
S. M. Shasha ◽  
O. S. Better ◽  
C. Chaimovitz ◽  
J. Doman ◽  
Y. Kishon
Keyword(s):  
Bile Duct ◽  
Bile Duct Ligation ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Significant Rise ◽  
Cirrhosis Of The Liver ◽  
Sodium Retention ◽  
Oedema Formation ◽  
Duct Ligation

1. Dogs with bile-duct ligation retain salt and water and form ascites. The present study was undertaken to examine the role of haemodynamic factors in the aetiology of this sodium retention. 2. Haemodynamic studies were performed in five dogs before and 5 weeks after bile-duct ligation. 3. After the operation there was an insignificant fall in mean arterial pressure, a significant rise in mean cardiac index and a significant fall in mean total peripheral resistance. 4. It is concluded that heart failure is not a factor in renal sodium retention of the dog with bile-duct ligation, since the central venous pressure was not elevated. 5. The haemodynamic pattern and the tendency to salt retention in the dog with chronic bile-duct ligation closely resemble findings reported in patients with cirrhosis of the liver, and it is suggested that oedema formation in patients with cirrhosis of the liver and dogs with chronic bile-duct ligation shares a common aetiology.

Bid-mediated apoptosis does not contribute to cholestatic liver injury following bile duct ligation

2009 ◽  
Vol 47 (01) ◽  
Author(s):  
P Nalapareddy ◽  
S Schüngel ◽  
MP Manns ◽  
H Jaeschke ◽  
A Vogel
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Bile Duct Ligation ◽  
Duct Ligation ◽  
Cholestatic Liver Injury

HGF/c-Met and IL-6/gp130 cooperatively regulate liver homeostasis and antibacterial signalling after bile-duct-ligation

2010 ◽  
Vol 48 (01) ◽  
Author(s):  
A Giebeler ◽  
S Erschfeld ◽  
C Birchmeier ◽  
C Trautwein ◽  
KL Streetz
Keyword(s):  
Bile Duct ◽  
Bile Duct Ligation ◽  
Duct Ligation

Adenoviral CCN3/NOV gene transfer fails to mitigate liver fibrosis in an experimental bile duct ligation model because of hepatocyte apoptosis

2012 ◽  
Vol 32 (9) ◽  
pp. 1342-1353 ◽  
Author(s):  
Erawan Borkham-Kamphorst ◽  
Sebastian Huss ◽  
Eddy Leur ◽  
Ute Haas ◽  
Ralf Weiskirchen
Keyword(s):  
Bile Duct ◽  
Gene Transfer ◽  
Liver Fibrosis ◽  
Bile Duct Ligation ◽  
Hepatocyte Apoptosis ◽  
Duct Ligation
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