ArticleDigestive diseases and sciences2001
Protective effect of ammonia against reflux esophagitis in rats.
Article in Digestive diseases and sciences, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Alpinumisoflavone ameliorates experimental acute reflux esophagitis in rats via regulation of inflammatory pathway.Acta cirurgica brasileira · 2025Article
- Helicobacter pylori Has an Inverse Relationship With Severity of Reflux Esophagitis.Journal of neurogastroenterology and motility · 2011Article
- Will symptomatic gastroesophageal reflux disease develop into reflux esophagitis?Journal of gastroenterology · 2006Article
- Gastroesophageal Reflux Disease: An Emerging Disease in Asia.Gastroenterology & hepatology · 2006Article
- Development of reflux esophagitis following Helicobacter pylori eradication.Journal of gastroenterology · 2005Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although several recent studies have reported that curing Helicobacter pylori (H. pylori) may result in the development of reflux esophagitis (RE), the mechanisms leading to this complication are unknown. One by product of H. pylori infection is ammonia, which serves as an acid neutralizer. The aim of this study was to clarify whether ammonia, which is produced during H. pylori infection, has a protective effect on the esophagus. Eight-week-old male Sprague-Dawley rats were fasted for 24 hrs. Under anesthesia, both the pylorus and limiting ridge were simultaneously ligated. One hour postligation, 0.3 ml of saline or ammonia at various concentrations was administered intragastrically by gastric intubation. Three hours after ligation, the animals were killed, the esophagus and stomach were removed, and the length of esophageal hemorrhagic erosions was measured. The incidence of RE was 100% (7/7) in the control group, 71% (5/7) in the low-ammonia group, 29% (2/7) in the middle-ammonia group, and 14% (1/7) in the high-ammonia group. The severity of lesions decreased in correspondence to increases in ammonia concentration. The development of RE was significantly inhibited by ammonia in a dose-dependent manner. This study indicates that ammonia protects against development of RE. A decreased amount of ammonia in the stomach might be related to the development of RE after H. pylori eradication therapy.
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