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[An experimental study on gastric mucosal damage induced by duodenogastric reflux in rats].

Jianxiang Liu, Xinguang Liu, Yun Dai, Xiuying Tang, Jiang Li, Huahong Wang

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Abstract

OBJECTIVE: Duodenogastric reflux (DGR) is an important factor causing gastric mucosal damage, but whether short-term DGR cause gastric damage and its characteristics remain unclear. The aim of the study is to investigate the damage of gastric mucosa and its characteristics due to short-term DGR in a rat model. METHODS: Healthy, male SD rats were divided into three groups: a DGR group, a pylorus ligation group and a control group. The rats were sacrificed three weeks after the operation. The damage of gastric mucosa was observed macroscopically and microscopically. The pH value and bilirubin level of the gastric fluid were examined. The tight junctions between antral mucosal cells were evaluated under transmission electronmicroscopy. The serum gastrin concentration was investigated with radioimmune assay. Myeloperoxidase (MPO) was examined with chemical method. RESULTS: Macroscopically, there were significant mucosal lesions such as erosions, ulcers and bleeding spots in the DGR group. Microscopically, short-term DGR can cause faveolar hyperplasia, but no apparent intestinal metaplasia and atrophy were observed. There was scarcely presence of acute and chronic inflammatory cell infiltration and MPO activity remained unchanged. The pH value and bilirubin level of gastric fluid increased significantly and the serum gastrin concentrations did not change a lot. Short-term DGR can cause destruction of tight junction, which was shorter in duration, less in deformation and might even disappear at the time of examination. CONCLUSIONS: It is suggested that short-term DGR can induce gastric damage, faveolar hyperplasia and tight junction destruction without inflammatory cell infiltration and MPO activity changes.

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What this paper is about

OBJECTIVE: Duodenogastric reflux (DGR) is an important factor causing gastric mucosal damage, but whether short-term DGR cause gastric damage and its characteristics remain unclear. The aim of the study is to investigate the damage of gastric mucosa and its characteristics due to short-term DGR in a rat model. METHODS: Healthy, male SD rats were divided into three groups: a DGR group, a pylorus ligation group and a control group. The rats were sacrificed three weeks after the operation. The damage of gastric mucosa was observed macroscopically and microscopically. The pH value and bilirubin level of the gastric fluid were examined. The tight junctions between antral mucosal cells were evaluated under transmission electronmicroscopy. The serum gastrin concentration was investigated with radioimmune assay. Myeloperoxidase (MPO) was examined with chemical method. RESULTS: Macroscopically, there were significant mucosal lesions such as erosions, ulcers and bleeding spots in the DGR group. Microscopically, short-term DGR can cause faveolar hyperplasia, but no apparent intestinal metaplasia and atrophy were observed. There was scarcely presence of acute and chronic inflammatory cell infiltration and MPO activity remained unchanged. The pH value and bilirubin level of gastric fluid increased significantly and the serum gastrin concentrations did not change a lot. Short-term DGR can cause destruction of tight junction, which was shorter in duration, less in deformation and might even disappear at the time of examination. CONCLUSIONS: It is suggested that short-term DGR can induce gastric damage, faveolar hyperplasia and tight junction destruction without inflammatory cell infiltration and MPO activity changes.

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Available abstract

OBJECTIVE: Duodenogastric reflux (DGR) is an important factor causing gastric mucosal damage, but whether short-term DGR cause gastric damage and its characteristics remain unclear. The aim of the study is to investigate the damage of gastric mucosa and its characteristics due to short-term DGR in a rat model. METHODS: Healthy, male SD rats were divided into three groups: a DGR group, a pylorus ligation group and a control group. The rats were sacrificed three weeks after the operation. The damage of gastric mucosa was observed macroscopically and microscopically. The pH value and bilirubin level of the gastric fluid were examined. The tight junctions between antral mucosal cells were evaluated under transmission electronmicroscopy. The serum gastrin concentration was investigated with radioimmune assay. Myeloperoxidase (MPO) was examined with chemical method. RESULTS: Macroscopically, there were significant mucosal lesions such as erosions, ulcers and bleeding spots in the DGR group. Microscopically, short-term DGR can cause faveolar hyperplasia, but no apparent intestinal metaplasia and atrophy were observed. There was scarcely presence of acute and chronic inflammatory cell infiltration and MPO activity remained unchanged. The pH value and bilirubin level of gastric fluid increased significantly and the serum gastrin concentrations did not change a lot. Short-term DGR can cause destruction of tight junction, which was shorter in duration, less in deformation and might even disappear at the time of examination. CONCLUSIONS: It is suggested that short-term DGR can induce gastric damage, faveolar hyperplasia and tight junction destruction without inflammatory cell infiltration and MPO activity changes.

Key concepts: Medicine, Gastroenterology, Internal medicine, Gastric mucosa, Pathology, Hyperplasia, Stomach, Myeloperoxidase

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[An experimental study on gastric mucosal damage induced by duodenogastric reflux in rats]. — Research Paper | ScholarLens