| Sphincter of Oddi dysfunction in hypercholesterolemic rabbits. | |
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MedLine Citation:
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PMID: 18301301 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND AND OBJECTIVES: The mechanisms that trigger gallbladder evacuation dysfunction, the key risk factor for gallstone formation, have not yet been fully elucidated. The sphincter of Oddi (SO) plays important roles in the regulation of gallbladder evacuation and maintenance of normal hydraulic pressure of the biliary tract. The aim of our study was to investigate the effects of hypercholesterolemia on the motility function of SO and the underlying mechanisms of SO dysfunction (SOD). METHODS: Forty New Zealand white rabbits were divided randomly into the control group fed with standard chow and the experimental (Ch) group fed with a high-cholesterol diet for 8 weeks. Changes in the maximal gallbladder emptying rate, gallbladder evacuation with cholecystokinin-octapeptide (CCK-8) stimulation and SO functions of both groups were measured in vivo; B ultrasound examination was used for dynamic observation of peristaltic movements in vivo; SO pressure was measured using manometry; morphological characteristics were observed by electronic microscope; laser scanning confocal fluorescence microscopy was used to identify changes in [Ca]i and Ca oscillation in primary SO smooth muscle cells (SMCs). RESULTS: Gallbladder cholestasis was observed during early stages of gallstone formation in Ch rabbits. CCK-8 could not improve the gallbladder cholestatic state in Ch group. Passive dilation of SO significantly improved the cholestatic state in Ch rabbits (P<0.05), although the maximal gallbladder emptying rate was still lower than that of the control group. Manometry data indicted a significant increase in the base pressure of the SO low-pressure ampulla segment and high-pressure segment (P<0.05) in Ch group. laser scanning confocal fluorescence microscopy assay data indicated that [Ca]i in SO cells of Ch group significantly increased and were in a state of overload (P<0.05); Ca oscillation signals in SO cells of Ch group were also abnormal. CONCLUSION: Hypercholesterolemia initially induced SOD, leading to increased gallbladder evacuation resistance and cholestasis. We suggested that [Ca]i overload and/or Ca oscillation abnormality potentially play important roles in the pathogenesis of SOD. |
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Authors:
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Xiao-Yong Zhang; Guang-Bin Cui; Ke-Jun Ma; Sha Wang; Ya-Ning Wei; Pang Du; Bao-Ying Chen; Wei Guo; Xin-Jiang Wang; Hai-Dong Huang; Jian-Hong Wang; Xiao-Feng Huang; Chun-Mei Wang; Yue-Min Wang; Jing-Guo Wei |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: European journal of gastroenterology & hepatology Volume: 20 ISSN: 1473-5687 ISO Abbreviation: Eur J Gastroenterol Hepatol Publication Date: 2008 Mar |
Date Detail:
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Created Date: 2008-02-27 Completed Date: 2009-04-03 Revised Date: 2009-10-16 |
Medline Journal Info:
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Nlm Unique ID: 9000874 Medline TA: Eur J Gastroenterol Hepatol Country: England |
Other Details:
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Languages: eng Pagination: 202-8 Citation Subset: IM |
Affiliation:
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Department of Radiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, China. zhang-xy@fmmu.edu.cn |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Bile / metabolism Calcium Signaling Cholecystography / methods Cholestasis / etiology, physiopathology Cholesterol / blood Cholesterol, Dietary / administration & dosage Disease Models, Animal Female Gallbladder Emptying Hypercholesterolemia / complications*, pathology, physiopathology Male Microscopy, Confocal / methods Peristalsis Rabbits Sincalide / diagnostic use Sphincter of Oddi / metabolism, ultrastructure Sphincter of Oddi Dysfunction / etiology*, pathology, physiopathology, radiography |
| Chemical | |
Reg. No./Substance:
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0/Cholesterol, Dietary; 25126-32-3/Sincalide; 57-88-5/Cholesterol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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