Role of Antidiuretic Hormone in Impaired Urinary Dilution Associated with Chronic Bile-Duct Ligation

1980 ◽  
Vol 58 (6) ◽  
pp. 493-500 ◽  
Author(s):  
O. S. Better ◽  
G. A. Aisenbrey ◽  
T. Berl ◽  
R. J. Anderson ◽  
W. A. Handelman ◽  
...  
Keyword(s):  
Bile Duct ◽  
Antidiuretic Hormone ◽  
Bile Duct Ligation ◽  
Diluting Segment ◽  
Water Excretion ◽  
Duct Ligation ◽  
Normal Mean ◽  
And Function ◽  
Distal Delivery

1. The effect of chronic bile-duct ligation on systemic and renal haemodynamics and on the capacity to dilute the urine was studied in conscious rats. Sham-operated rats served as controls. 2. In the rats with bile-duct ligation, the maximal urinary diluting capacity was impaired, despite an expanded plasma volume, a normal mean arterial pressure and cardiac output, and normal intrarenal determinants of water excretion including distal delivery of fluid and function of the diluting segment. 3. In contrast, maximal urinary dilution capacity was intact in rats with congenital central diabetes insipidus and chronic bile-duct ligation. 4. It is concluded that the defect in urinary dilution in rats with chronic bile-duct ligation is dependent on antidiuretic hormone.

Paclitaxel alleviates liver fibrosis induced by bile duct ligation in rats: Role of TGF-β1, IL-10 and c-Myc

Life Sciences ◽  
2018 ◽  
Vol 211 ◽  
pp. 245-251 ◽  
Author(s):  
Maha H. Sharawy ◽  
Noha Abdel-Rahman ◽  
Nirmeen Megahed ◽  
Mohammed S. El-Awady
Keyword(s):  
Bile Duct ◽  
Liver Fibrosis ◽  
Bile Duct Ligation ◽  
Duct Ligation ◽  
Tgf Β1

scholarly journals Melatonin regulates L-arginine transport and NADPH oxidase in young rats with bile duct ligation: role of protein kinase C

2013 ◽  
Vol 73 (1-4) ◽  
pp. 395-401 ◽  
Author(s):  
You-Lin Tain ◽  
Chih-Cheng Chen ◽  
Chien-Te Lee ◽  
Ying-Hsien Kao ◽  
Jiunn-Ming Sheen ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Bile Duct ◽  
Protein Kinase ◽  
Nadph Oxidase ◽  
Bile Duct Ligation ◽  
Arginine Transport ◽  
Young Rats ◽  
Kinase C ◽  
Duct Ligation

Altered hepatobiliary permeability induced by Amanita phalloides in the rat and the protective role of bile duct ligation

1981 ◽  
Vol 58 (3) ◽  
pp. 370-378 ◽  
Author(s):  
Carolyn L. Fuhrman-Lane ◽  
Chesley P. Erwin ◽  
James M. Fujimoto ◽  
Martyn J. Dibben
Keyword(s):  
Bile Duct ◽  
Bile Duct Ligation ◽  
Protective Role ◽  
Amanita Phalloides ◽  
Duct Ligation

scholarly journals Loss of cellular FLICE-inhibitory protein promotes acute cholestatic liver injury and inflammation from bile duct ligation

2018 ◽  
Vol 314 (3) ◽  
pp. G319-G333 ◽  
Author(s):  
Nadine Gehrke ◽  
Michael Nagel ◽  
Beate K. Straub ◽  
Marcus A. Wörns ◽  
Marcus Schuchmann ◽  
...  
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Bile Acids ◽  
Bile Duct Ligation ◽  
Ex Vivo ◽  
Mapk Signaling ◽  
Caspase 8 ◽  
Duct Ligation ◽  
Cholestatic Liver Injury

Cholestatic liver injury results from impaired bile flow or metabolism and promotes hepatic inflammation and fibrogenesis. Toxic bile acids that accumulate in cholestasis induce apoptosis and contribute to early cholestatic liver injury, which is amplified by accompanying inflammation. The aim of the current study was to evaluate the role of the antiapoptotic caspase 8-homolog cellular FLICE-inhibitory (cFLIP) protein during acute cholestatic liver injury. Transgenic mice exhibiting hepatocyte-specific deletion of cFLIP (cFLIP−/−) were used for in vivo and in vitro analysis of cholestatic liver injury using bile duct ligation (BDL) and the addition of bile acids ex vivo. Loss of cFLIP in hepatocytes promoted acute cholestatic liver injury early after BDL, which was characterized by a rapid release of proinflammatory and chemotactic cytokines (TNF, IL-6, IL-1β, CCL2, CXCL1, and CXCL2), an increased presence of CD68+ macrophages and an influx of neutrophils in the liver, and resulting apoptotic and necrotic hepatocyte cell death. Mechanistically, liver injury in cFLIP−/− mice was aggravated by reactive oxygen species, and sustained activation of the JNK signaling pathway. In parallel, cytoprotective NF-κB p65, A20, and the MAPK p38 were inhibited. Increased injury in cFLIP−/− mice was accompanied by activation of hepatic stellate cells and profibrogenic regulators. The antagonistic caspase 8-homolog cFLIP is a critical regulator of acute, cholestatic liver injury. NEW & NOTEWORTHY The current paper explores the role of a classical modulator of hepatocellular apoptosis in early, cholestatic liver injury. These include activation of NF-κB and MAPK signaling, production of inflammatory cytokines, and recruitment of neutrophils in response to cholestasis. Because these signaling pathways are currently exploited in clinical trials for the treatment of nonalcoholic steatohepatitis and cirrhosis, the current data will help in the development of novel pharmacological options in these indications.

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