| Esophageal injury with external esophageal perfusion. | |
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MedLine Citation:
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PMID: 15921698 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: External esophageal perfusion (EEP) with the idea that esophageal perfusion can be controlled with a single ingredient at a constant rate and concentration, might be used to dissect the injurious role of gastro-duodenal secretions for the progression from esophagitis to Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). This study is to evaluate the EEP rat model for esophagitis induced by using a micro-osmotic pump with bile perfusion. METHODS: Eighteen adult rats underwent the EEP procedure. Bile (0.5% bovine bile, pH 7.4) was used as perfusion agent and three types of perfusions were performed: 1 week perfusion, 2 weeks perfusion, and 4 weeks perfusion compared to saline perfusion and sham operation. Histological changes, cell proliferation, apoptosis, 8-hydroxy-deoxyguanosine (8-OH-dG) and Manganese superoxide dismutase (MnSOD) were observed after perfusion and compared. RESULTS: The bile perfusion for 1 week, 2 weeks, and 4 weeks induced mucosa infiltration of inflammatory cells, basal cell hyperproliferation, and papillae hypertrophy in all animals. Histopathology and cellular changes consistent with the findings associated with reflux esophagitis. The apoptotic index, the proliferating index, and expression of 8-OH-dG were significantly increased in the esophageal mucosa compared to controls. MnSOD expression was decreased with bile perfusion compared to saline controls. CONCLUSIONS: The external esophageal perfusion model enabled precise control of the injurious agent. It induced the typical histological injury and cellular changes seen in severe reflux esophagitis. The cellular changes in apoptosis, proliferation and anti-oxidant defense make this model unique for reflux esophagitis studies. Further studies are needed to induce Barrett's esophagus and esophageal adenocarcinoma. |
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Authors:
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Yan Li; John M Wo; Ruifeng R Su; Mukunda B Ray; Whitney Jones; Robert C G Martin |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of surgical research Volume: 129 ISSN: 0022-4804 ISO Abbreviation: J. Surg. Res. Publication Date: 2005 Nov |
Date Detail:
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Created Date: 2005-10-24 Completed Date: 2005-12-09 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0376340 Medline TA: J Surg Res Country: United States |
Other Details:
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Languages: eng Pagination: 107-13 Citation Subset: IM |
Affiliation:
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Division of Surgical Oncology, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis Bile* / chemistry Cell Division Deoxyguanosine / analogs & derivatives, analysis Esophagitis, Peptic / pathology* Esophagus / chemistry, pathology* Gastric Juice / chemistry Hypertrophy Immunohistochemistry In Situ Nick-End Labeling Mucous Membrane / pathology Perfusion* Rats Rats, Sprague-Dawley Superoxide Dismutase / analysis Time Factors |
| Chemical | |
Reg. No./Substance:
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0/8-hydroxy-2'-deoxyguanosine; 961-07-9/Deoxyguanosine; EC 1.15.1.1/Superoxide Dismutase |
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