1129 Esophageal Bolus Volume-Dependent Upper Esophageal Sphincter (UES) and Lower Esophageal Sphincter (LES) Reflexes in Infants with Birth Asphyxia

2016 ◽  
Vol 150 (4) ◽  
pp. S228
Author(s):  
Theresa Shubert ◽  
Swetha Sitaram ◽  
Sudarshan Jadcherla
Keyword(s):  
Lower Esophageal Sphincter ◽  
Birth Asphyxia ◽  
Upper Esophageal Sphincter ◽  
Bolus Volume ◽  
Esophageal Sphincter

scholarly journals The Effect of Bolus Volume on Hyoid Kinematics in Healthy Swallowing

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Ahmed Nagy ◽  
Sonja M. Molfenter ◽  
Melanie Péladeau-Pigeon ◽  
Shauna Stokely ◽  
Catriona M. Steele
Keyword(s):  
Peak Velocity ◽  
Upper Esophageal Sphincter ◽  
Healthy Population ◽  
Bolus Volume ◽  
Velocity Increase ◽  
Movement Distance ◽  
Hyoid Movement ◽  
Laryngeal Vestibule ◽  
Esophageal Sphincter ◽  
Liquid Bolus

Hyoid movement in swallowing is biomechanically linked to closure of the laryngeal vestibule for airway protection and to opening of the upper esophageal sphincter. Studies suggest that the range of hyoid movement is highly variable in the healthy population. However, other aspects of hyoid movement such as velocity remain relatively unexplored. In this study, we analyze data from a sample of 20 healthy young participants (10 male) to determine whether hyoid movement distance, duration, velocity, and peak velocity vary systematically with increases in thin liquid bolus volume from 5 to 20 mL. The temporal correspondence between peak hyoid velocity and laryngeal vestibule closure was also examined. The results show that maximum hyoid position and peak velocity increase significantly for 20 mL bolus volumes compared to smaller volumes, and that the timing of peak velocity is closely linked to achieving laryngeal vestibule closure. This suggests that generating hyoid movements with increased power is a strategy for handling larger volumes.

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 ◽  
...  
Keyword(s):  
Lower Esophageal Sphincter ◽  
Upper Esophageal Sphincter ◽  
Esophageal Sphincter

Esophageal manometry in the opossum.

1977 ◽  
Vol 233 (3) ◽  
pp. E152
Author(s):  
K Schulze ◽  
W J Dodds ◽  
J Christensen ◽  
J D Wood
Keyword(s):  
Animal Model ◽  
Lower Esophageal Sphincter ◽  
Esophageal Manometry ◽  
Lower Esophageal Sphincter Pressure ◽  
Upper Esophageal Sphincter ◽  
Sphincter Pressure ◽  
Coronal Section ◽  
Esophageal Sphincter ◽  
Human Esophagus

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.

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.

Effect of prostaglandin E2 on esophageal motility in man

1975 ◽  
Vol 39 (3) ◽  
pp. 479-481 ◽  
Author(s):  
A. Mukhopadhyay ◽  
S. Rattan ◽  
R. K. Goyal
Keyword(s):  
Prostaglandin E2 ◽  
Lower Esophageal Sphincter ◽  
Esophageal Motility ◽  
Lower Esophageal Sphincter Pressure ◽  
Upper Esophageal Sphincter ◽  
The Body ◽  
Inhibitory Influence ◽  
Sphincter Pressure ◽  
Esophageal Sphincter ◽  
Peristaltic Contractions

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.

M1200 Effect of Pharyngeal Stimulus on Upper Esophageal Sphincter (UES) and Lower Esophageal Sphincter (LES) During Development in Human Pre-Term Infants

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

Biomechanics of failed deglutitive upper esophageal sphincter relaxation in neurogenic dysphagia

2002 ◽  
Vol 283 (1) ◽  
pp. G16-G26 ◽  
Author(s):  
Rohan B. H. Williams ◽  
Karen L. Wallace ◽  
Galib N. Ali ◽  
Ian J. Cook
Keyword(s):  
Biomechanical Properties ◽  
Upper Esophageal Sphincter ◽  
Zenker’S Diverticulum ◽  
Bolus Volume ◽  
Neurogenic Dysphagia ◽  
Zenker's Diverticulum ◽  
Pharyngeal Swallow ◽  
Extrapyramidal Disease ◽  
Esophageal Sphincter ◽  
Ues Opening

Our aims were to examine the etiology and biomechanical properties of the nonrelaxing upper esophageal sphincter (UES) and the relationship between UES opening and failed relaxation. We examined the relationships among swallowed bolus volume, intrabolus pressure, sagittal UES diameter, the pharyngeal swallow response, and geniohyoid shortening in 18 patients with failed UES relaxation, 23 healthy aged controls, and 15 with Zenker's diverticulum. Etiology of failed UES relaxation was 56% medullary disease, 33% Parkinson's or extrapyramidal disease; and 11% idiopathic. Extent of UES opening ranged from absent to normal and correlated with preservation of the pharyngeal swallow response ( P = 0.012) and geniohyoid shortening ( P = 0.046). Intrabolus pressure was significantly greater compared with aged controls ( P < 0.001) or Zenker's diverticulum ( P < 0.001). The bolus volume-dependent increase in intrabolus pressure evident in controls was not observed in failed UES relaxation. The nonrelaxing UES therefore displays a constant loss of sphincter compliance throughout the full, and potentially normal, range of expansion during opening. Adequacy of UES opening is influenced by the degree of preservation of the pharyngeal swallow response and hyolaryngeal traction. In contrast, the stenotic UES displays a static loss of compliance, only apparent once the limit of sphincter expansion is reached.

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