ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2014
Mechanism of UES relaxation initiated by gastric air distension.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Retrograde cricopharyngeus dysfunction (R-CPD), also known as inability to belch syndrome-a narrative review.Translational gastroenterology and hepatology · 2026Review
- Biomechanical effects of esophageal elongation on the circumferential tension of the cervical esophagus in vivo.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- A biomechanical response of the esophagus participates in swallowing.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Pepsin concentration in oral lavage fluid of rabbit reflux model constructed by dilating the lower esophageal sphincter.Open medicine (Warsaw, Poland) · 2023Article
- Retrograde upper esophageal sphincter function… and dysfunction.Neurogastroenterology and motility · 2022Article
- The effect of body position on esophageal reflexes in cats: a possible mechanism of SIDS?Pediatric research · 2018Article
- Characterization and mechanisms of the supragastric belch in the cat.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Characterization and mechanisms of the pharyngeal swallow activated by stimulation of the esophagus.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- The Physiology of Eructation.Dysphagia · 2016Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The aim of this study was to determine the mechanism of initiation of transient upper esophageal sphincter relaxation (TUESR) caused by gastric air distension. Cats (n = 31) were decerebrated, EMG electrodes were placed on the cricopharyngeus, a gastric fistula was formed, and a strain gauge was sewn on the lower esophageal sphincter (n = 8). Injection of air (114 ± 13 ml) in the stomach caused TUESR (n = 18) and transient lower esophageal sphincter relaxation (TLESR, n = 6), and this effect was not significantly (P > 0.05) affected by thoracotomy. Free air or bagged air (n = 6) activated TLESR, but only free air activated TUESR. Closure of the gastroesophageal junction blocked TUESR (9/9), but not TLESR (4/4), caused by air inflation of the stomach. Venting air from distal esophagus during air inflation of the stomach prevented TUESR (n = 12) but did not prevent air escape from the stomach to the esophagus (n = 4). Rapid injection of air on the esophageal mucosa always caused TUESR (9/9) but did not always (7/9) cause an increase in esophageal pressure. The time delay between the TUESR and the rapid air pulse was significantly more variable (P < 0.05) than the time delay between the rapid air pulse and the rise in esophageal pressure. We concluded that the TUESR caused by gastric air distension is dependent on air escape from the stomach, which stimulates receptors in the esophagus, but is not dependent on distension of the stomach or esophagus, or the TLESR. Therefore, the TUESR caused by gastric air distension is initiated by stimulation of receptors in the esophageal mucosa.
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Registered trials
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