Esophageal injury with external esophageal perfusion

被引:18
作者
Li, Y
Wo, JM
Su, RFR
Ray, MB
Jones, W
Martin, RCG
机构
[1] Univ Louisville, Div Surg Oncol, Sch Med, James Graham Brown Canc Ctr, Louisville, KY 40202 USA
[2] Univ Louisville, Sch Med, Div Gastroenterol Hepatol, Louisville, KY 40202 USA
[3] Univ Louisville, Sch Med, Dept Anat Pathol, Louisville, KY 40202 USA
关键词
gastroesophageal reflux; esophagitis; animal model; oxidative stress;
D O I
10.1016/j.jss.2005.04.018
中图分类号
R61 [外科手术学];
学科分类号
摘要
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 mirco-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 bypertrophy 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 esolphagitis. The cellular changes in apoptosis, proliferatilon and anti-oxidant defense make this model unique for reflux esophagitis studies. Further studies are needed to induce Barrett's esophagus and esophageal adenocarcinoma. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:107 / 113
页数:7
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