scholarly journals Upper esophageal sphincter during transient lower esophageal sphincter relaxation: effects of reflux content and posture

2010 ◽  
Vol 298 (5) ◽  
pp. G601-G607 ◽  
Author(s):  
Arash Babaei ◽  
Valmik Bhargava ◽  
Ravinder K. Mittal
Keyword(s):  
Lower Esophageal Sphincter ◽  
Esophageal Pressure ◽  
Upper Esophageal Sphincter ◽  
Pressure Increase ◽  
Major Influence ◽  
High Resolution Manometry ◽  
Relaxation Effects ◽  
Lower Esophageal Sphincter Relaxation ◽  
Esophageal Sphincter ◽  
The Right

Although some studies show that the upper esophageal sphincter (UES) contracts during transient lower esophageal sphincter relaxation (TLESR), others show that it relaxes. We hypothesized that the posture of the subject and constituents of gastroesophageal reflux (GER) may determine the type of UES response during the TLESR. High-resolution manometry and esophageal pH/impedance recording were performed in 10 healthy volunteers in the right recumbent (1 h) and upright (1 h) positions following the ingestion of a 1,000-Kcal meal. The UES pressure response during TLESR and constituents of GER (liquid, air, and pH) were determined. 109 TLESRs (58 upright and 51 recumbent) were analyzed. The majority of TLESRs were associated with GER (91% upright and 88% recumbent) events. UES relaxation was the predominant response during upright position (81% of TLESRs), and it was characteristically associated with presence of air in the reflux (92%). On the other hand, UES contraction was the predominant response during recumbent position (82% of TLESRs), and it was mainly associated with liquid reflux (71%). The rate of esophageal pressure increase (dP/d t) during the GER, but not the pH, had major influence on the type of UES response during TLESR. The dP/d t during air reflux (127 ± 39 mmHg/s) was significantly higher than liquid reflux (31 ± 6 mmHg/s, P < 0.0001). We concluded that the nature of UES response during TLESR, relaxation or contraction, is related to the posture and the constituents of GER. We propose that the rapid rate of esophageal pressure increase associated with air reflux determines the UES relaxation response to GER.

Upper esophageal sphincter function during gastroesophageal reflux events revisited

2000 ◽  
Vol 279 (2) ◽  
pp. G262-G267 ◽  
Author(s):  
Silvia Torrico ◽  
Mark Kern ◽  
Muhammad Aslam ◽  
Subashini Narayanan ◽  
Ananda Kannappan ◽  
...  
Keyword(s):  
Gastroesophageal Reflux ◽  
Esophageal Pressure ◽  
Upper Esophageal Sphincter ◽  
Pressure Increase ◽  
Sphincter Function ◽  
Average Percentage ◽  
Control Subjects ◽  
Asymptomatic Volunteers ◽  
Esophageal Sphincter ◽  
Intraesophageal Pressure

Upper esophageal sphincter (UES) function during gastroesophageal reflux events is not completely elucidated because previous studies addressing this issue yielded conflicting results. We reexamined the UES pressure response to intraluminal esophageal pressure and pH changes induced by reflux events. We studied 14 healthy, asymptomatic volunteers (age 49 ± 6 yr) and 7 gastroesophageal reflux disease patients (age 48 ± 5 yr). UES pressure, intraesophageal pressure, and pH were monitored at the distal, middle, and proximal esophagus concurrently in the supine position 1 h before and 2 h after a 1,000-calorie meal. A total of 321 reflux events were identified by the development of abrupt reflux-induced intraesophageal pressure increase (IPI); 285 events occurred in patients and 36 in control subjects. In control subjects 33 of 36 and in patients 252 of 285 IPI events were associated with a pH drop. Among patients and control subjects, 99% and 100%, respectively, of all IPI events irrespective of pH drop were associated with abrupt increase in UES pressure (34 ± 2 and 27 ± 6 mmHg, respectively). The average percentage of maximum UES pressure increase over prereflux values ranged between 66% and 96% (control subjects) and 34% and 122% (patients). IPIs induced by both acidic and nonacidic reflux events evoke strong UES contractile responses.

scholarly journals Mechanism of UES relaxation initiated by gastric air distension

2014 ◽  
Vol 307 (4) ◽  
pp. G452-G458 ◽  
Author(s):  
Ivan M. Lang ◽  
Bidyut K. Medda ◽  
Reza Shaker
Keyword(s):  
Time Delay ◽  
Lower Esophageal Sphincter ◽  
Gastroesophageal Junction ◽  
Esophageal Pressure ◽  
Upper Esophageal Sphincter ◽  
Gastric Fistula ◽  
Esophageal Mucosa ◽  
Rapid Injection ◽  
Free Air ◽  
Esophageal Sphincter

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.

scholarly journals A novel pattern of longitudinal muscle contraction with subthreshold pharyngeal stimulus: a possible mechanism of lower esophageal sphincter relaxation

2012 ◽  
Vol 302 (5) ◽  
pp. G542-G547 ◽  
Author(s):  
Eric Leslie ◽  
Valmik Bhargava ◽  
Ravinder K. Mittal
Keyword(s):  
Muscle Contraction ◽  
Lower Esophageal Sphincter ◽  
Motor Neurons ◽  
Longitudinal Muscle ◽  
Upper Esophageal Sphincter ◽  
Distal Esophagus ◽  
High Resolution Manometry ◽  
Proximal Esophagus ◽  
Strong Contraction ◽  
Esophageal Sphincter

A subthreshold pharyngeal stimulus induces lower esophageal sphincter (LES) relaxation and inhibits progression of ongoing peristaltic contraction in the esophagus. Recent studies show that longitudinal muscle contraction of the esophagus may play a role in LES relaxation. Our goal was to determine whether a subthreshold pharyngeal stimulus induces contraction of the longitudinal muscle of the esophagus and to determine the nature of this contraction. Studies were conducted in 16 healthy subjects. High resolution manometry (HRM) recorded pressures, and high frequency intraluminal ultrasound (HFIUS) images recorded longitudinal muscle contraction at various locations in the esophagus. Subthreshold pharyngeal stimulation was induced by injection of minute amounts of water in the pharynx. A subthreshold pharyngeal stimulus induced strong contraction and caudal descent of the upper esophageal sphincter (UES) along with relaxation of the LES. HFIUS identified longitudinal muscle contraction of the proximal (3–5 cm below the UES) but not the distal esophagus. Pharyngeal stimulus, following a dry swallow, blocked the progression of dry swallow-induced peristalsis; this was also associated with UES contraction and descent along with the contraction of longitudinal muscle of the proximal esophagus. We identify a unique pattern of longitudinal muscle contraction of the proximal esophagus in response to subthreshold pharyngeal stimulus, which we propose may be responsible for relaxation of the distal esophagus and LES through the stretch sensitive activation of myenteric inhibitory motor neurons.

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