Renal and Cardiovascular Effects of Chronic Occlusion of the Bile Duct in Rats

Keeler, R.

doi:10.1159/000182210

Cited by 4 publications

(4 citation statements)

References 14 publications

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“…In fact, the BDL model is characterized by poliuria [6,7], which is of uncertain origin. Possibly, the hyperbilirubinaemia or the elevated levels of bile acids are responsible for this alteration in water handling.…”

Section: Discussionmentioning

confidence: 99%

“…Several groups of authors have studied the cardiovascular and renal alterations that occur in this model [3][4][5][6][7][8], which reproduces some of the features of human cirrhosis. Thus chronic BDL induces a circulatory hyperdynamic state, with arterial hypotension and increased cardiac output, similar to that found in other experimental models of cirrhosis and in cirrhotic patients.…”

Section: Introductionmentioning

confidence: 99%

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Haemodynamic and renal evolution of the bile duct-ligated rat

et al. 2000

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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.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Haemodynamic and renal evolution of the bile duct-ligated rat

et al. 2000

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“…Levels of NO and endothelial NO synthase (eNOS) protein expression are increased in aortic and pulmonary tissue, contributing to the vasodilation in those tissues (3,5,22). However, in the renal circulation, the site of vasoconstriction and reduced renal blood flow (RBF) during CBDL-induced cirrhosis (11,12,13,26), it is reasonable to hypothesize that eNOS protein expression and locally produced NO are decreased. In addition, recent studies have demonstrated that while NO is central to the vascular dysfunction during cirrhosis, there is a significant NO-independent component that contributes to the vascular dysfunction (2,3).…”

mentioning

confidence: 99%

Decreased renal heme oxygenase-1 expression contributes to decreased renal function during cirrhosis

Miyazono

Garat

Carter

2002

American Journal of Physiology-Renal Physiology

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Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme, catalyzing the oxidative cleavage of heme molecules to biliverdin, carbon monoxide, and iron. The present study was designed to investigate the role of HO-1 in the pathogenesis of renal dysfunction during cirrhosis. Biliary cirrhosis was induced in rats by common bile duct ligation (CBDL). Animals were studied 2 and 5 wk after surgery. In kidney from CBDL rats, HO-1 protein expression increased slightly at 2 wk but was abolished at 5 wk. In addition, we confirmed histologically that HO-1 expression was suppressed in renal tubules and interlobular arterioles in 5-wk-old CBDL rats. Conversely, HO-1 expression in liver was strongly increased. Consistent with the development of cirrhosis and renal dysfunction mean arterial pressure (MAP), glomerular filtration rate (GFR), and renal blood flow (RBF) were decreased in CBDL rats compared with sham-operated controls. In sham rats, treatment with the selective HO inhibitor zinc protoporphyrin markedly decreased GFR and RBF to values similar to those measured in CBDL rats without decreasing MAP. In conclusion, decreased renal HO-1 expression contributes to deteriorated renal function and hemodynamics during cirrhosis. This finding provides a novel mechanism for the pathophysiology of renal dysfunction during cirrhosis.

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“…volume, and splanchnic blood flow, and decreased peripheral resistance that leads to a decreased mean arterial pressure (MAP) [1]. Yet, despite the hyperdynamic circulation and prominent peripheral vasodilation, the renal vasculature is markedly vasoconstricted and renal sodium and water handling is impaired [2][3][4][5][6][7][8][9][10]. Because these alterations can precipitate many of the complications of liver disease, much effort has been aimed at elucidating the potential mechanisms that lead to the renal dysfunction.…”

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confidence: 99%