Effects of Bronchial Obstruction on Lower Esophageal Sphincter Motility and Gastroesophageal Reflux in Patients with Asthma

2002 ◽  
Vol 166 (9) ◽  
pp. 1206-1211 ◽  
Author(s):  
Frank Zerbib ◽  
Olivier Guisset ◽  
Hervé Lamouliatte ◽  
André Quinton ◽  
Jean Paul Galmiche ◽  
...  
Keyword(s):  
Gastroesophageal Reflux ◽  
Lower Esophageal Sphincter ◽  
Bronchial Obstruction ◽  
Esophageal Sphincter

Food and Gastroesophageal Reflux Disease

2019 ◽  
Vol 26 (19) ◽  
pp. 3497-3511 ◽  
Author(s):  
Teodora Surdea-Blaga ◽  
Dana E. Negrutiu ◽  
Mariana Palage ◽  
Dan L. Dumitrascu
Keyword(s):  
Gastroesophageal Reflux Disease ◽  
Gastroesophageal Reflux ◽  
Lower Esophageal Sphincter ◽  
Reflux Disease ◽  
Current Knowledge ◽  
Positive Association ◽  
Sphincter Pressure ◽  
Low Carbohydrate Diet ◽  
Reflux Symptoms ◽  
Esophageal Sphincter

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.

Triggering of transient LES relaxations in ferrets: role of sympathetic pathways and effects of baclofen

2000 ◽  
Vol 279 (1) ◽  
pp. G157-G162 ◽  
Author(s):  
Esther Staunton ◽  
Scott D. Smid ◽  
John Dent ◽  
L. Ashley Blackshaw
Keyword(s):  
Gastroesophageal Reflux ◽  
Lower Esophageal Sphincter ◽  
Glucose Infusion ◽  
Gastric Distention ◽  
Low Level ◽  
Before And After ◽  
Esophageal Sphincter ◽  
Splanchnic Mechanoreceptors ◽  
High Level

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.

Gastroesophageal Reflux and Prokinetic Agents

2005 ◽  
Vol 24 (2) ◽  
pp. 51-58 ◽  
Author(s):  
Davita Hammer
Keyword(s):  
Weight Gain ◽  
Gastroesophageal Reflux ◽  
Lower Esophageal Sphincter ◽  
Preterm Infants ◽  
Aspiration Pneumonia ◽  
Main Mechanism ◽  
Term Infants ◽  
Gastric Contents ◽  
Esophageal Sphincter ◽  
Poor Weight Gain

GASTROESOPHAGEAL REFLUX (GER), a common problem in preterm and term infants, occurs when there is retrograde movement of gastric contents into the esophagus. The severity of the reflux is related to the height of the gastric contents up into the esophagus or the oral pharynx. Transient lower esophageal sphincter relaxation is the main mechanism thought to be responsible for GER in infants.1–3In a study conducted by Marino and associates, approximately 60 percent of preterm infants were affected by reflux.4GER is associated with irritability, apnea and bradycardia, poor weight gain, aspiration pneumonia, and esophagitis.2,5–7

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