Sumatriptan maintains the post-prandial increase in transient lower esophageal sphincter relaxations and increases gastroesophageal reflux in normal subjects

1998 ◽  
Vol 114 ◽  
pp. A838
Author(s):  
D. Sifrim ◽  
RH Holloway ◽  
T Missotten ◽  
A Zelter ◽  
J Tack ◽  
...  
2002 ◽  
Vol 282 (6) ◽  
pp. G1052-G1058 ◽  
Author(s):  
John E. Pandolfino ◽  
Guoxiang Shi ◽  
Jennifer Curry ◽  
Raymond J. Joehl ◽  
James G. Brasseur ◽  
...  

To quantify the effect of hiatus hernia (HH) on esophagogastric junction (EGJ) distensibility, eight normal subjects and nine gastroesophageal reflux disease (GERD) patients with HH were studied with concurrent manometry, fluoroscopy, and stepwise controlled barostatic distention of the EGJ. The minimal barostatic pressure required to open the EGJ during the interswallow period was determined. Thereafter, barium swallows were imaged in 5-mmHg increments of intrabag pressure. EGJ diameter and length were measured at each pressure during deglutitive relaxation. The EGJ opening diameter was greater in hernia patients compared with normal subjects during deglutitive relaxation at all pressures, and EGJ length was 23% shorter. EGJ opening pressure among hernia patients was lower than normal subjects during the interswallow period. In conclusion, the EGJ of GERD patients with HH was more distensible and shorter than normal subjects. These findings partially explain why HH patients are predisposed to reflux by mechanisms other than transient lower esophageal sphincter relaxations, sustain greater volumes of refluxate, and have a reduced ability to discriminate gas from liquid reflux.


2019 ◽  
Vol 26 (19) ◽  
pp. 3497-3511 ◽  
Author(s):  
Teodora Surdea-Blaga ◽  
Dana E. Negrutiu ◽  
Mariana Palage ◽  
Dan L. Dumitrascu

Gastroesophageal reflux disease is a chronic condition with a high prevalence in western countries. Transient lower esophageal sphincter relaxation episodes and a decreased lower esophageal sphincter pressure are the main mechanisms involved. Currently used drugs are efficient on reflux symptoms, but only as long as they are administered, because they do not modify the reflux barrier. Certain nutrients or foods are generally considered to increase the frequency of gastroesophageal reflux symptoms, therefore physicians recommend changes in diet and some patients avoid bothering foods. This review summarizes current knowledge regarding food and gastroesophageal reflux. For example, fat intake increases the perception of reflux symptoms. Regular coffee and chocolate induce gastroesophageal reflux and increase the lower esophageal exposure to acid. Spicy foods might induce heartburn, but the exact mechanism is not known. Beer and wine induce gastroesophageal reflux, mainly in the first hour after intake. For other foods, like fried food or carbonated beverages data on gastroesophageal reflux is scarce. Similarly, there are few data about the type of diet and gastroesophageal reflux. Mediterranean diet and a very low carbohydrate diet protect against reflux. Regarding diet-related practices, consistent data showed that a “short-meal-to-sleep interval” favors reflux episodes, therefore some authors recommend that dinner should be at least four hours before bedtime. All these recommendations should consider patient’s weight, because several meta-analyses showed a positive association between increased body mass index and gastroesophageal reflux disease.


2002 ◽  
Vol 166 (9) ◽  
pp. 1206-1211 ◽  
Author(s):  
Frank Zerbib ◽  
Olivier Guisset ◽  
Hervé Lamouliatte ◽  
André Quinton ◽  
Jean Paul Galmiche ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A244
Author(s):  
Jianmin Liu ◽  
James L. Puckett ◽  
Nonko Pehlivanov ◽  
Ravinder K. Mittal

2000 ◽  
Vol 279 (1) ◽  
pp. G157-G162 ◽  
Author(s):  
Esther Staunton ◽  
Scott D. Smid ◽  
John Dent ◽  
L. Ashley Blackshaw

Activation of gastric vagal mechanoreceptors by distention is thought to be the trigger for transient lower esophageal sphincter relaxations (TLESR), which lead to gastroesophageal reflux. The contribution of higher-threshold gastric splanchnic mechanoreceptors is uninvestigated. GABABreceptor agonists, including baclofen, potently reduce triggering of TLESR by low-level gastric distention. We aimed to determine first whether this effect of baclofen is maintained at high-level distention and second the role of splanchnic pathways in triggering TLESR. Micromanometric/pH studies in conscious ferrets showed that intragastric glucose infusion (25 ml) increased triggering of TLESR and reflux. Both were significantly reduced by baclofen (7 μmol/kg ip) ( P < 0.05). When 40 ml of air was added to the glucose infusion, more TLESR occurred than with glucose alone ( P < 0.01). These were also reduced by baclofen ( P < 0.001). TLESR after glucose/air infusion were assessed before and after splanchnectomy (2–4, 9–11, and 23–25 days), which revealed no change. Baclofen inhibits TLESR after both low- and high-level gastric distention. Splanchnic pathways do not contribute to increased triggering of TLESR by high-level gastric distention.


Sign in / Sign up

Export Citation Format

Share Document