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.

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.

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.

Electroacupuncture attenuates vascular hyporeactivity in a rat model of portal hypertension induced by bile duct ligation

2021 ◽  
pp. 096452842110392
Author(s):  
Yu-Sheng Chen ◽  
Chorng-Kai Wen ◽  
Geng-Hao Liu ◽  
Tzung-Yan Lee
Keyword(s):  
Portal Hypertension ◽  
Growth Factor ◽  
Bile Duct ◽  
Bile Duct Ligation ◽  
Portal Pressure ◽  
Contractile Responses ◽  
Hyperdynamic Circulation ◽  
Duct Ligation ◽  
Tnf Α ◽  
Cox 1

Background: A hyperdynamic circulation and impaired vascular responsiveness to vasoconstrictors are observed in portal hypertension (PHT) rats. Inflammation is a major contributor to the hyperdynamic circulation state in murine models of PHT. Electroacupuncture (EA) may ameliorate the inflammatory response and limit arterial vasodilatation and portal pressure. This study investigated the possible mechanisms underlying putative hemodynamics effects of EA in normal and PHT rats. Methods: PHT was induced by bile duct ligation (BDL) surgery over 4 weeks in rats. Sham-operated and BDL rats were treated with low-frequency EA (2 Hz) at ST36 10 min three times weekly for one or two consecutive weeks (for a total of 3 or 7 treatments, respectively). Serum tumor necrosis factor-α (TNF-α), nitrite/nitrate (NOx) and 6-keto-prostaglandin F1α (6-keto-PGF1α) were analyzed, and hemodynamic variation and contractile responses to phorbol-12,13-dibutyrate and phenylephrine in aortic and superior mesenteric arterial rings were recorded. Inducible (i) and endothelial (3) nitric oxide synthase (NOS), cyclooxygenase-1 (COX-1), and protein kinase C-α (PKC-α) levels were determined by Western blotting. Results: EA significantly reduced portal pressure and serum TNF-α, NOx and 6-keto-PGF1α levels compared to the untreated BDL group, enhanced maximum contractile responses in the aorta, up-regulated PKC-α, and down-regulated iNOS and COX-1 levels. In addition, EA decreased the aortic angiogenesis signaling cascade, reflected by down-regulation of vascular endothelial growth factor (VEGF) abundance and transforming growth factor β receptor (TGFβR)I/II expression, as assessed by immunostaining. Conclusion: EA attenuates TNF-α, NO and 6-keto-PGF1α overproduction, modulates the vascular levels of constitutive NOS and PKC-α, blunts the development of the angiogenesis cascade, and enhances vascular contractile force in PHT rats.

Early Fibrotic Injury in A Rat Model of Bile Duct Ligation: Further Evidence of Intrinsic Matrix Metalloproteinase 8

2012 ◽  
Vol 172 (2) ◽  
pp. 244-245
Author(s):  
S.S. Ciullo ◽  
C.S. Muratore ◽  
Y. Zhou ◽  
T.F. Tracy
Keyword(s):  
Bile Duct ◽  
Matrix Metalloproteinase ◽  
Rat Model ◽  
Bile Duct Ligation ◽  
Duct Ligation

scholarly journals Human Chorionic Plate-Derived Mesenchymal Stem Cells Restore Hepatic Lipid Metabolism in a Rat Model of Bile Duct Ligation

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yun Bin Lee ◽  
Jong Ho Choi ◽  
Eun Nam Kim ◽  
Jin Seok ◽  
Hyun-Jung Lee ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Lipid Metabolism ◽  
Bile Duct ◽  
Rat Model ◽  
Liver Diseases ◽  
Bile Duct Ligation ◽  
Expression Levels ◽  
Duct Ligation ◽  
Chorionic Plate

In cholestatic liver diseases, impaired bile excretion disrupts lipid homeostasis. We investigated changes of lipid metabolism, including mitochondrial β-oxidation, in a rat model of bile duct ligation (BDL) in which chorionic plate-derived mesenchymal stem cells (CP-MSCs) were transplanted. Serum cholesterol level, which was elevated after BDL, was significantly decreased following CP-MSC transplantation. The expression levels of genes involved in intracellular lipid uptake, including long-chain fatty acyl-CoA synthetases and fatty acid transport proteins, were decreased in rats after BDL; however, they were not significantly changed by subsequent CP-MSC transplantation. Carnitine palmitoyltransferase 1A (CPT1A), a rate-limiting enzyme in mitochondrial β-oxidation, was upregulated after BDL and then was downregulated after CP-MSC transplantation. CPT1A expression was changed via microRNA-33—a posttranscriptional regulator of CPT1A—in a peroxisome proliferator-activated receptor α-independent manner. Cellular adenosine triphosphate production—an indicator of mitochondrial function—was reduced after BDL and was restored by CP-MSC transplantation. Expression levels of heme oxygenases also were significantly affected following BDL and CP-MSC transplantation. Lipid metabolism is altered in response to chronic cholestatic liver injury and can be restored by CP-MSC transplantation. Our study findings support the therapeutic potential of CP-MSCs in cholestatic liver diseases and help in understanding the fundamental mechanisms by which CP-MSCs affect energy metabolism.

Common bile duct ligation in the rat: a model of intrapulmonary vasodilatation and hepatopulmonary syndrome

1997 ◽  
Vol 272 (4) ◽  
pp. G779-G784 ◽  
Author(s):  
M. B. Fallon ◽  
G. A. Abrams ◽  
J. W. McGrath ◽  
Z. Hou ◽  
B. Luo
Keyword(s):  
Portal Hypertension ◽  
Bile Duct ◽  
Gas Exchange ◽  
Common Bile Duct ◽  
Lung Injury ◽  
Bile Duct Ligation ◽  
Hepatopulmonary Syndrome ◽  
Common Bile Duct Ligation ◽  
Arterial Blood ◽  
Duct Ligation

Hepatopulmonary syndrome (HPS) causes impaired oxygenation due to intrapulmonary vasodilatation in patients with cirrhosis. Chronic common bile duct ligation (CBDL) in the rat results in gas-exchange abnormalities similar to HPS, but intrapulmonary vasodilatation has not been evaluated. We assess intrapulmonary vasodilatation, measured in vivo, after CBDL. Sham, 2- and 5-wk CBDL, and 3-wk partial portal vein ligated (PVL) rats had hepatic and lung injury, portal pressure, and arterial blood gases assessed. The pulmonary microcirculation was evaluated by injecting microspheres (size range 5.5-10 microm) intravenously and measuring the size and number of microspheres bypassing the lungs in arterial blood. CBDL animals developed progressive hepatic injury and portal hypertension accompanied by gas-exchange abnormalities and intrapulmonary vasodilatation. PVL animals, with a similar degree of portal hypertension, did not develop intrapulmonary vasodilatation or abnormal gas exchange. No lung injury was observed. CBDL, but not PVL, causes progressive intrapulmonary vasodilatation, which accompanies worsening arterial gas exchange. These findings validate CBDL as a model to study HPS.

Early colchicine administration reduces hepatic fibrosis and portal hypertension in rats with bile duct ligation

1993 ◽  
Vol 19 (1) ◽  
pp. 90-94 ◽  
Author(s):  
Jorge L. Poo ◽  
Gérard Feldmann ◽  
Alain Moreau ◽  
Christophe Gaudin ◽  
Didier Lebrec
Keyword(s):  
Portal Hypertension ◽  
Bile Duct ◽  
Hepatic Fibrosis ◽  
Bile Duct Ligation ◽  
Duct Ligation
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