Lower Esophageal Sphincter (LES) Hypertension Influences Intraesophageal (ILP) and Upper Esophageal Sphincter (UES) Pressures in Achalasic Patients

2005 ◽  
Vol 61 (5) ◽  
pp. AB136
Author(s):  
Michele Marchese ◽  
Cristiano Spada ◽  
Andrea Tringali ◽  
Pietro Familiari ◽  
Lucio Petruzziello ◽  
...  
1977 ◽  
Vol 233 (3) ◽  
pp. E152
Author(s):  
K Schulze ◽  
W J Dodds ◽  
J Christensen ◽  
J D Wood

The opossum esophagus is commonly used as an animal model of the human esophagus. We used esophageal manometry in normal animals to provide basal data about normal esophageal motor functions in vivo in this species. At rest, separate and distinct high pressure zones can be recorded at the level of the lower esophageal sphincter, diaphragmatic hiatus, aortic arch, and upper esophageal sphincter. Each zone demonstrates a characteristic pattern of pressures in the radii of the coronal section and a characteristic response to swallowing. The hiatal and aortic zones can be mistaken for the esophageal sphincters. Pressures in the sphincters fall with swallowing. Peristalsis is not bolus-dependent and occurs with 98% of swallows. Pressures generated by peristalsis are greater in the middle of the esophagus than at the ends. Values for resting lower esophageal sphincter pressure and the characteristics of peristalsis were reproducible between different studies in the same animals.


2014 ◽  
Vol 307 (4) ◽  
pp. G452-G458 ◽  
Author(s):  
Ivan M. Lang ◽  
Bidyut K. Medda ◽  
Reza Shaker

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.


1975 ◽  
Vol 39 (3) ◽  
pp. 479-481 ◽  
Author(s):  
A. Mukhopadhyay ◽  
S. Rattan ◽  
R. K. Goyal

Studies were performed to investigate the effect of prostaglandin E2 on esophageal motility in 12 healthy volunteers. PGE2 infusion caused a dose-dependent reduction in the lower esophageal sphincter pressure. The threshold dose was less than 0.05 mug-kg-1-min-1 and maximal reduction of pressure (60%) occurred with a dose of 0.4 mug-kg-1-min-1. In contrast to its effect on the lower esophageal sphincter, PGE2 did not alter the pressure in the upper esophageal sphincter. PGE2 did not influence resting esophageal pressures; the amplitude of peristaltic contractions was reduced in the lower but not in the upper part of the body of the esophagus. These studies show that in man PGE2 exerts selective inhibitory influence on the activity of the lower part of the esophagus and lower esophageal sphincter which are composed of smooth muscle fibers.


2010 ◽  
Vol 138 (5) ◽  
pp. S-353
Author(s):  
Sudarshan R. Jadcherla ◽  
Vanessa N. Parks ◽  
Juan Peng ◽  
Soledad A. Fernandez ◽  
Reza Shaker

2012 ◽  
Vol 302 (5) ◽  
pp. G542-G547 ◽  
Author(s):  
Eric Leslie ◽  
Valmik Bhargava ◽  
Ravinder K. Mittal

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.


2010 ◽  
Vol 298 (5) ◽  
pp. G601-G607 ◽  
Author(s):  
Arash Babaei ◽  
Valmik Bhargava ◽  
Ravinder K. Mittal

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.


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