Establishment of Surgically Induced Chronic Acid Reflux Esophagitis in Rats

Omura, Hiromi

doi:10.1080/003655299750025020

Cited by 93 publications

(21 citation statements)

References 8 publications

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“…The experimental protocol was approved by the Animal Care and Use Committee of the Osaka City University. Acid reflux esophagitis was induced by the method reported by Omura et al [24]. In brief, the duodenum near the pyloric ring was covered with a 2-mm wide piece of an 18-Fr Nélaton catheter (Terumo Co, Tokyo, Japan), and the transitional region between the forestomach and the glandular portion was ligated to enhance reflux of gastric contents into the esophagus (Figure 1A).…”

Section: Methodsmentioning

confidence: 99%

Acid Reflux Directly Causes Sleep Disturbances in Rat with Chronic Esophagitis

et al. 2014

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Background & AimsGastroesophageal reflux disease (GERD) is strongly associated with sleep disturbances. Proton pump inhibitor (PPI) therapy improves subjective but not objective sleep parameters in patients with GERD. This study aimed to investigate the association between GERD and sleep, and the effect of PPI on sleep by using a rat model of chronic acid reflux esophagitis.MethodsAcid reflux esophagitis was induced by ligating the transitional region between the forestomach and the glandular portion and then wrapping the duodenum near the pylorus. Rats underwent surgery for implantation of electrodes for electroencephalogram and electromyogram recordings, and they were transferred to a soundproof recording chamber. Polygraphic recordings were scored by using 10-s epochs for wake, rapid eye movement sleep, and non-rapid eye movement (NREM) sleep. To examine the role of acid reflux, rats were subcutaneously administered a PPI, omeprazole, at a dose of 20 mg/kg once daily.ResultsRats with reflux esophagitis presented with several erosions, ulcers, and mucosal thickening with basal hyperplasia and marked inflammatory infiltration. The reflux esophagitis group showed a 34.0% increase in wake (232.2±11.4 min and 173.3±7.4 min in the reflux esophagitis and control groups, respectively; p<0.01) accompanied by a reduction in NREM sleep during light period, an increase in sleep fragmentation, and more frequent stage transitions. The use of omeprazole significantly improved sleep disturbances caused by reflux esophagitis, and this effect was not observed when the PPI was withdrawn.ConclusionsAcid reflux directly causes sleep disturbances in rats with chronic esophagitis.

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Section: Methodsmentioning

confidence: 99%

Acid Reflux Directly Causes Sleep Disturbances in Rat with Chronic Esophagitis

et al. 2014

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“…The control group (sham-operated) rats were operated with only midline incision and digital manipulation of the stomach. In experimental group (7D-ligated), chronic reflux esophagitis was developed by following the methods as described earlier (Omura et al 1999). In brief, the abdomen was opened by giving a 3- to 4-cm-long midline incision and latex ring (2 mm in thickness; ID, 5–6 mm; OD, 8–9 mm) made from 18-Fr Nalaton catheter was placed around the area of pyloric sphincter in order to restrict gastric emptying.…”

Section: Methodsmentioning

confidence: 99%

Altered expression of P2X3 in vagal and spinal afferents following esophagitis in rats

Banerjee

Medda

Schmidt

et al. 2009

Histochem Cell Biol

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Purinergic P2X3 receptors are predominantly expressed in small diameter primary afferent neurons and activation of these receptors by adenosine triphosphate is reported to play an important role in nociceptive signaling. The objective of this study was to investigate the expression of P2X3 receptors in spinal and vagal sensory neurons and esophageal tissues following esophagitis in rats. Two groups of rats were used including 7 days fundus-ligated (7D-ligated) esophagitis and sham-operated controls. Esophagitis was produced by ligating the fundus and partial obstruction of pylorus that initiated reflux of gastric contents. The sham-operated rats underwent midline incision without surgical manipulation of the stomach. Expressions of P2X3 receptors in thoracic dorsal root ganglia (DRGs), nodose ganglia (NGs), and esophageal tissues were evaluated by RT–PCR, western blot and immunohistochemistry. Esophageal neurons were identified by retrograde transport of Fast Blue from the esophagus. There were no significant differences in P2X3 mRNA expressions in DRGs (T1–T3) and NGs between 7D-ligated and sham-operated rats. However, there was an upregulation of P2X3 mRNA in DRGs (T6–T12) and in the esophageal muscle. At protein level, P2X3 exhibited significant upregulation both in DRGs and in NGs of rats having chronic esophagitis. Immunohistochemical analysis exhibited a significant increase in P2X3 and TRPV1 co-expression in DRGs and NGs in 7D-ligated rats compared to sham-operated rats. The present findings suggest that chronic esophagitis results in upregulation of P2X3 and its co-localization with TRPV1 receptor in vagal and spinal afferents. Changes in P2X3 expression in vagal and spinal sensory neurons may contribute to esophageal hypersensitivity following acid reflux-induced esophagitis.

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“…Chronic acid reflux esophagitis was induced by the methods of Omura et al [17]. In brief, the duodenum near the pylorus was covered with a piece of 18-Fr Nélaton catheter (width, 2 mm; Sapheed ® , Terumo Co., Tokyo, Japan) as a ring, and the transitional region between the forestomach and the glandular portion was ligated with 2–0 silk thread to enhance reflux of gastric acid into the esophagus.…”

Section: Methodsmentioning

confidence: 99%

“…Recently, Omura et al [17]established a rat chronic reflux esophagitis model, which exhibited thickness of the epithelium with elongation of lamina papillae and leukocyte infiltration. These histological findings are similar to those of patients with reflux esophagitis, and treatment with lansoplazole prevented development of esophagitis, suggesting that the changes associated with this model were mainly caused by acid reflux.…”

Section: Introductionmentioning

confidence: 99%

Increased Expression of Cytokines and Adhesion Molecules in Rat Chronic Esophagitis

et al. 2003

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Background/Aims: Cytokines and adhesion molecules regulate many inflammatory processes in several gastrointestinal diseases. The dynamics of cytokines and adhesion molecules in reflux esophagitis are unknown in detail. We examined the expression and dynamics of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α), MIP-2, GRO/cytokine-induced neutrophil chemoattractant-2α (CINC-2α), intercellular adhesion molecule-1 (ICAM-1), leukocyte function-associated antigen 1 (LFA-1; CD11a/CD18), and Mac-1 (CD11b/CD18) in rat chronic reflux esophagitis. Methods: Chronic acid reflux esophagitis was induced in Wistar rats by ligating the transitional region between the forestomach and the glandular portion and wrapping the duodenum near the pylorus with a small piece of an 18-Fr Nélaton catheter. Rats were killed 3 or 21 days after operation. The levels of mRNA expression of cytokines and ICAM-1 were determined by real-time quantitative RT-PCR. Localization of adhesion molecules and cytokines was investigated by immunohistochemical staining, and numbers of LFA-1- or Mac-1-positive cells were quantified. Results: IL-1β, TNF-α, MCP-1, MIP-1α, MIP-2, CINC-2α, and ICAM-1 mRNA expression was significantly increased in esophageal lesions compared with normal esophagus. There were few these cytokines- or adhesion molecule-positive cells in normal esophagus. In regions of esophagitis, numerous inflammatory leukocytes in lamina propria and the submucosal layer exhibited positive reactions for these cytokines and endothelial cells were intensely stained for ICAM-1. Numbers of LFA-1- and Mac-1-positive cells were significantly increased in rat chronic esophagitis. Treatment with rabeprazole almost completely inhibited development of chronic acid reflux esophagitis and significantly decreased expression of cytokines and ICAM-1 mRNA in esophageal tissue compared with control. Conclusion: Cytokines and adhesion molecules play important roles in the pathogenesis of chronic reflux esophagitis in this rat model.

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Establishment of Surgically Induced Chronic Acid Reflux Esophagitis in Rats

Abstract: This experimental rat model is considered useful as a model of chronic acid-type esophagitis for the evaluation of the pathophysiology of reflux esophagitis and the evaluation of drug efficacy.

Cited by 93 publications

References 8 publications

Acid Reflux Directly Causes Sleep Disturbances in Rat with Chronic Esophagitis

Acid Reflux Directly Causes Sleep Disturbances in Rat with Chronic Esophagitis

Altered expression of P2X3 in vagal and spinal afferents following esophagitis in rats

Increased Expression of Cytokines and Adhesion Molecules in Rat Chronic Esophagitis

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