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Upper esophageal sphincter (UES) pressure changes during transient lower esophageal sphincter relaxation (TLESR). Most patients with gastroesophageal reflux show an increase in UES pressure during TLESR. However, many controls exhibit no UES pressure changes during TLESR. GERD, gastroesophageal reflux disease.

Upper esophageal sphincter (UES) pressure changes during transient lower esophageal sphincter relaxation (TLESR). Most patients with gastroesophageal reflux show an increase in UES pressure during TLESR. However, many controls exhibit no UES pressure changes during TLESR. GERD, gastroesophageal reflux disease.

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Transient lower esophageal sphincter relaxation (TLESR) is the main mechanism of gastroesophageal reflux disease (GERD). The aim of this study was to investigate the characteristics of transient lower esophageal sphincter movement in patients with or without gastroesophageal reflux by high-resolution manometry (HRM). From June 2010 to July 2010, we...

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... with GERD showed primarily increasing UES pressure during TLESR. Twenty-five TLESR (75.8%) events revealed increasing UES pressure in the GERD group. However, only six were associated with increasing UES pressure in the control group. The frequency of increasing UES pressure differed between the groups (P = 0.001) (Fig. 2). The percen- tages of UES relaxation were 21.2% in the GERD group and 73.5% in the control group (P = ...

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... Although the variability in frequency of TLESRs varies in different studies from 0 to 12 TLESRs/hour. [27,28] Both studies included both complete and incomplete TLESRs. To our knowledge this is the first study that analyzed the number of TLESRs after ARMS. ...
... -ASA classification of III or higher. Health-related QoL GERD 28 (21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32) Brief dysphagia questionnaire (BEDQ) 7 (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14) Displayed as n(%), mean ± SD or median with IQR. HRM; high resolution manometry ...
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... Decrease in UES pressure during transient lower esophageal sphincter relaxation was observed in 21.2% of GERD patients and in 73.5% of controls. 29 Electromyographic analysis of the cricopharyngeal muscle in GERD patients did not show differences as compared with findings in healthy volunteers. 30 Also, a study assessing esophageal striated muscle contractions by manometry did not show different results between GERD patients with and without esophagitis. ...
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Introduction The upper esophageal sphincter (UES) is a muscular structure located at the transition from the pharynx to the esophagus, with the cricopharyngeal muscle as the most important component. During gastroesophageal reflux, the pressure in the UES elevates, which is apparently a protective mechanism to prevent esophagopharyngeal reflux and airway aspiration. In gastroesophageal reflux disease (GERD), there may be functional changes in the UES. Objective The objective of the present review was to determine UES functional changes in GERD. Data Synthesis In healthy individuals, gastroesophageal reflux causes an increase in the UES pressure. This response of the sphincter is at least partially impaired in patients with GERD. In the disease, the UES has a reduced length and decreased resting pressure. However, other publications found that in chronic gastroesophageal reflux the basal sphincter pressure increase, differences which may be consequent to the measurement method or to disease severity. The UES opening during swallowing has a smaller diameter, and the bolus transit time through the sphincter is longer. Conclusion The UES of patients with GERD does not open as expected and the bolus flow through the sphincter is longer. This behavior may be associated with dysphagia, a frequent complaint in patients with GERD.
... One of the most widely postulated mechanisms for the development of reflux symptoms is excess transient lower esophageal sphincter relaxation (TLESR) episodes. 30 These episodes are physiologic processes that allow for venting of gastric gas and act as protection against the accumulation of excess gas in the stomach. 30 TLESRs are vasovagally induced reflexes that are triggered by gastric distention and work via several neurotransmitters and receptors, including the GABA B receptor. ...
... 30 These episodes are physiologic processes that allow for venting of gastric gas and act as protection against the accumulation of excess gas in the stomach. 30 TLESRs are vasovagally induced reflexes that are triggered by gastric distention and work via several neurotransmitters and receptors, including the GABA B receptor. 31 Through its GABA B receptor activity, baclofen inhibits TLESRs, and has been shown to significantly inhibit gastroesophageal reflux disease (GERD) episodes in both healthy volunteers and in patients with reflux disease. ...
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... A similar behavior occurs during transient lower esophageal sphincter relaxation (tLESR). This spontaneous relaxation of the LES periodically allows air trapped in the stomach to escape [43]. Following this type of opening in the model presented here, the lighter fluid is then able to increase the area of the sphincter and enter the esophageal lumen as shown in Fig. 7f. ...
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... They found that patients with GERD were more likely to demonstrate UES contraction during tLOSRs than controls, who more frequently displayed UES relaxation. This phenomenon is hypothesized to be due to the more acidic refluxate in patients with GERD (23). ...
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... Also, in cases of incomplete TLESR, LES elevation is seen with HRM manometry, and ultrasonography shows esophageal muscle thickening 2 cm above the LES, indicating contraction of the esophageal longitudinal muscle, which may be the main cause of TLESR. 11 Hypotensive lower esophageal sphincter, crural diaphragmatic dysfunction, or increased esophagogastric junction compliance without abnormal anatomy LES pressure in normal individuals is lowest after eating and highest at night. Even if the LES is relaxed, the pressure remains slightly higher than the intragastric pressure, to prevent reflux. ...
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Gastroesophageal reflux disease (GERD) is a very common disease, and the prevalence in the general population has recently increased. GERD is a chronic relapsing disease associated with motility disorders of the upper gastrointestinal tract. Several factors are implicated in GERD, including hypotensive lower esophageal sphincter, frequent transient lower esophageal sphincter relaxation, esophageal hypersensitivity, reduced resistance of the esophageal mucosa against the refluxed contents, ineffective esophageal motility, abnormal bolus transport, deficits initiating secondary peristalsis, abnormal response to multiple rapid swallowing, and hiatal hernia. One or more of these mechanisms result in the reflux of stomach contents into the esophagus, delayed clearance of the refluxate, and the development of symptoms and/or complications. New techniques, such as 24-hour pH and multichannel intraluminal impedance monitoring, multichannel intraluminal impedance and esophageal manometry, high-resolution manometry, 3-dimensional highresolution manometry, enoscopic functional luminal imaging probe, and 24-hour dynamic esophageal manometry, provide more information on esophageal motility and have clarified the pathophysiology of GERD. Proton pump inhibitors remain the preferred pharmaceutical option to treat GERD. The ideal target of GERD treatment is to restore esophageal motility and reconstruct the antireflux mechanism. This review focuses on current advances in esophageal motor dysfunction in patients with GERD and the influence of these developments on GERD treatment.
... Disruption of the gastroesophageal barrier also occurs during transient lower esophageal sphincter relaxations (TLESRs) during which the LES relaxes to release excess gas from the stomach. TLESRs occur in the setting of gastric distention, which stimulates a vasovagal reflex and LES relaxation (11). Gastric distention may be secondary to ingestion of food or air and is exacerbated by alterations in gastric motility, which may be affected by type of oral intake and medications. ...
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... It is also considered to be one of the major mechanisms of gastroesophageal reflux in GERD patients (Dent et al., 1980). In comparison to healthy individuals, the frequency of Transient LES relaxation is obviously upregulated in GERD patients (Kim et al., 2013). Recently developed high-resolution manometry has revealed that Transient LES relaxation exerts longitudinal muscle contraction of the esophageal body and relaxation of the LES ( Babaei et al., 2008). ...
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Prostaglandin E2 (PGE2) plays a role in the pathogenesis of gastro-esophageal reflux disease (GERD). There are 4 subtypes of PGE2, PGE2 receptor 1, 2, 3 and 4 (EP 1-4). In GERD patents, PGE2, EP2 and EP4 are upregulated. However, the effects of PGE2 on esophageal motility remain elusive. We examined how PGE2 regulates motility in the porcine circular smooth muscle of the lower esophageal sphincter (LES), and the circular and longitudinal smooth muscle of the esophagus body in organ bath. PGE2 induced tonic relaxation in the LES and circular smooth muscle, but transient contraction in longitudinal smooth muscle. The relaxation of the LES and circular smooth muscle was similar in pattern and mechanism, but was much larger in the LES. The relaxation was completely blocked by a voltage-gated K+ channel blocker or 40 mM K+ depolarization, indicating the involvement of K+ channel. Longitudinal smooth muscle contraction was completely blocked by an L-type Ca2+ channel blocker, showing the contribution of Ca2+ movement. The involvement of the EP receptor in motility was examined with selective receptor agonists and antagonists. Activation of EP2 and EP4 caused relaxation in the LES and circular smooth muscle. Compatible with PGE2, EP2 and EP4 agonists caused more significant relaxation in the LES than in circular smooth muscle. EP1 contributed to the longitudinal smooth muscle contraction. The different effects of PGE2 in the LES, circular and longitudinal smooth muscle contributes to esophageal motility, their impairment might increase the amount and frequency of esophageal reflux.
... Under physiological conditions, these TLESRs are induced spontaneously without swallowing and allow for the "physiological" contact of gastric juice containing hydrochloric acid (HCl) with the esophageal wall [10]. Interestingly, this acid reflux occurs at a higher frequency during TLESR in patients with GERD than in healthy subjects [10,11]. Furthermore, the anatomical abnormalities in the structure of the lower esophageal sphincter or its dysfunction can result in more frequent or sometimes prolonged exposure of the esophageal mucosa to gastric acid, resulting in esophageal damage due to reflux esophagitis. ...
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