Document Detail

Hydrophilic but not hydrophobic bile acids prevent gallbladder muscle dysfunction in acute cholecystitis.
MedLine Citation:
PMID:  12774024     Owner:  NLM     Status:  MEDLINE    
The pathogenesis of acute cholecystitis (AC) is controversial. Bile acids may be involved in the pathogenesis of AC because the hydrophobic chenodeoxycholic acid (CDCA) reproduced in vitro the muscle dysfunction observed in AC and was prevented by the hydrophilic ursodeoxycholic acid (UDCA). The present study examined the in vivo effects of UDCA or CDCA on gallbladder muscle dysfunction caused by AC. Guinea pigs were treated with placebo, UDCA, or CDCA for 2 weeks before sham operation or induction of AC by bile duct ligation (BDL) for 3 days. Pretreatment with oral UDCA prevented the defective contraction in response to agonists (acetylcholine [ACh], cholecystokinin 8 [CCK-8], and KCl) that occurs after BDL. Prostaglandin (PG) E(2)-induced contraction remained normal in the placebo and UDCA-treated groups but was impaired in the CDCA-treated group. Treatment with UDCA also prevented the expected increase in the levels of H(2)O(2), lipid peroxidation, and PGE(2) content in the placebo-treated AC group, whereas CDCA caused further increases in these oxidative stress markers. The binding capacity of PGE(2) to its receptors and the activity of catalase were reduced after treatment with CDCA. Treatment with UDCA enriched gallbladder bile acids with its conjugates and reduced the percentage of CDCA conjugates. In contrast, treatment with CDCA significantly decreased the percentage of UDCA in bile. In conclusion, oral treatment with UDCA prevents gallbladder muscle damage caused by BDL, whereas oral treatment with CDCA worsens the defective muscle contractility and the oxidative stress.
Zuo-Liang Xiao; Piero Biancani; Martin C Carey; Jose Behar
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Hepatology (Baltimore, Md.)     Volume:  37     ISSN:  0270-9139     ISO Abbreviation:  Hepatology     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-05-29     Completed Date:  2003-06-18     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8302946     Medline TA:  Hepatology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1442-50     Citation Subset:  IM    
Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, RI, USA.
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MeSH Terms
Acetylcholine / pharmacology
Acute Disease
Bile / metabolism
Bile Acids and Salts / metabolism
Bile Ducts
Biological Markers / analysis
Catalase / antagonists & inhibitors
Chenodeoxycholic Acid / metabolism,  pharmacology*
Cholecystitis / etiology,  physiopathology*
Dinoprostone / antagonists & inhibitors,  metabolism,  pharmacology
Gallbladder / drug effects,  physiopathology*
Guinea Pigs
Hydrogen Peroxide / antagonists & inhibitors
Lipid Peroxides / antagonists & inhibitors
Muscle Contraction / drug effects
Muscle, Smooth / drug effects,  physiopathology*
Oxidative Stress / physiology
Receptors, Prostaglandin E / metabolism
Sincalide / pharmacology
Ursodeoxycholic Acid / metabolism,  pharmacology*
Grant Support
Reg. No./Substance:
0/Bile Acids and Salts; 0/Biological Markers; 0/Lipid Peroxides; 0/Receptors, Prostaglandin E; 128-13-2/Ursodeoxycholic Acid; 25126-32-3/Sincalide; 363-24-6/Dinoprostone; 474-25-9/Chenodeoxycholic Acid; 51-84-3/Acetylcholine; 7722-84-1/Hydrogen Peroxide; EC

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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