Provocation of transient lower esophageal sphincter relaxations by gastric distension with air

2001 ◽  
Vol 96 (8) ◽  
pp. 2317-2323 ◽  
Author(s):  
J W A Straathof ◽  
J Ringers ◽  
C B H W Lamers ◽  
A A M Masclee
Keyword(s):  
Lower Esophageal Sphincter ◽  
Gastric Distension ◽  
Esophageal Sphincter

Effect of hyperglycemia on triggering of transient lower esophageal sphincter relaxations

2004 ◽  
Vol 286 (5) ◽  
pp. G797-G803 ◽  
Author(s):  
Qing Zhang ◽  
Michael Horowitz ◽  
Rachael Rigda ◽  
Christopher Rayner ◽  
Andrew Worynski ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Lower Esophageal Sphincter ◽  
Blood Glucose Concentration ◽  
Gastric Wall ◽  
Gastric Distension ◽  
Healthy Human ◽  
Patients With Diabetes ◽  
Esophageal Sphincter ◽  
Volume Controlled ◽  
Pressure Controlled

Acute changes in blood glucose concentration have major effects on gastrointestinal motor function. Patients with diabetes mellitus have an increased prevalence of gastroesophageal reflux. Transient lower esophageal sphincter (LES) relaxation (TLESR) is the most common sphincter mechanism underlying reflux. The aim of this study was to investigate the effect of acute hyperglycemia on triggering TLESRs evoked by gastric distension in healthy volunteers. TLESRs were stimulated by pressure-controlled and volume-controlled (500 ml) gastric distension using an electronic barostat and performed on separate days. On each day, esophageal manometry was performed in the sitting position during gastric distension for 1 h under euglycemia (5 mM), and either marked hyperglycemia (15 mM) or physiological hyperglycemia (8 mM) in randomized order was maintained by a glucose clamp. Marked hyperglycemia doubled the rate of TLESRs in response to both pressure-controlled [5 (3–10.5, median or interquartile range) to 10 (9.5–14.5) per hour, P < 0.02] and volume-controlled [4 (2.5–7.5) to 10.5 (7–12.5) per hour, P < 0.02] gastric distension but had no effect on basal LES pressure. Physiological hyperglycemia had no effect on the triggering of TLESRs or basal LES pressure. In healthy human subjects, marked hyperglycemia increases the rate of TLESRs. Increase in the rate of TLESRs is independent of proximal gastric wall tension. Mechanisms underlying the effect remain to be determined. Hyperglycemia may be an important factor contributing to the increased esophageal acid exposure in patients with diabetes mellitus.

Diaphragmatic contribution to gastroesophageal competence and reflux in dogs

1992 ◽  
Vol 263 (4) ◽  
pp. G551-G557 ◽  
Author(s):  
C. J. Martin ◽  
W. J. Dodds ◽  
H. H. Liem ◽  
R. O. Dantas ◽  
R. D. layman ◽  
...  
Keyword(s):  
Gastroesophageal Reflux ◽  
Lower Esophageal Sphincter ◽  
Short Duration ◽  
Gastroesophageal Junction ◽  
Selective Inhibition ◽  
High Amplitude ◽  
Gastric Distension ◽  
Esophageal Body ◽  
Esophageal Sphincter ◽  
Crural Diaphragm

Events associated with gastroesophageal reflux have been determined by concurrent diaphragmatic and esophageal body electromyography, video radiography, and manometry in four conscious dogs. Three characteristic phenomena occurred in parallel immediately before and during gastroesophageal reflux: 1) transient lower esophageal sphincter relaxation, 2) profound (99.5%) and selective inhibition of crural diaphragmatic activity, and 3) a previously unrecognized dorsal movement of the gastroesophageal junction (mean 1.3 cm) demonstrated by implanted radiological markers. The patterns associated with spontaneous acid and gas reflux were indistinguishable from those induced by gastric distension. Costolumbar diaphragmatic activity was stable up until the instant of sphincter opening, when there was a single costolumbar contraction of short duration and high amplitude. Esophageal shortening did not occur before reflux. Reflux that occurred after atropine-induced inhibition of lower esophageal sphincter tone to < 2 mmHg was intermittent and coincided with selective crural inhibition. These studies demonstrated that selective crural inhibition is a prerequisite for gastroesophageal reflux and suggest that the crural diaphragm is an important factor for the maintenance of gastroesophageal competence.

H. pylori and transient lower esophageal sphincter relaxations induced by gastric distension in healthy humans

2001 ◽  
Vol 281 (2) ◽  
pp. G350-G356 ◽  
Author(s):  
Frank Zerbib ◽  
Valérie Bicheler ◽  
Véronique Leray ◽  
Madeleine Joubert ◽  
Stanislas Bruley des Varannes ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Lower Esophageal Sphincter ◽  
Proinflammatory Cytokine ◽  
Healthy Subjects ◽  
Gastric Distension ◽  
Healthy Humans ◽  
Biopsy Specimens ◽  
Esophageal Sphincter ◽  
H Pylori

The role of Helicobacter pylori infection in the control of lower esophageal sphincter (LES) motility, especially the occurrence of transient LES relaxations (TLESRs), was studied in eight H. pylori-positive and eight H. pylori-negative healthy subjects. During endoscopy, biopsy specimens were taken from the cardia, fundus, and antrum for determinations of H. pyloristatus, gastritis, and proinflammatory cytokine mucosal concentrations. LES motility was monitored during three different 30-min periods: baseline, gastric distension (barostat), and gastric distension with CCK infusion. Gastric distension significantly increased the TLESR rate, whereas CCK increased the rate of distension-induced TLESRs further and reduced resting LES pressure without significant differences between infected and noninfected subjects. H. pylori status did not influence resting LES pressure or gastric compliance. Cytokine mucosal concentrations were increased in infected patients, but no correlation was found with the TLESR rate, which was also independent of inflammation at the cardia, fundus, and antrum. These results suggest that H. pylori-associated inflammation does not affect the motor events involved in the pathogenesis of gastroesophageal reflux.

The Impact of Gastric Distension on the Lower Esophageal Sphincter and Its Exposure to Acid Gastric Juice

2010 ◽  
Vol 252 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Shahin Ayazi ◽  
Anand Tamhankar ◽  
Steven R. DeMeester ◽  
Joerg Zehetner ◽  
Calvin Wu ◽  
...  
Keyword(s):  
Gastric Juice ◽  
Lower Esophageal Sphincter ◽  
Gastric Distension ◽  
Esophageal Sphincter ◽  
The Impact

scholarly journals Gastric mechanosensory and lower esophageal sphincter function in rumination syndrome

1998 ◽  
Vol 275 (2) ◽  
pp. G314-G321 ◽  
Author(s):  
Miriam Thumshirn ◽  
Michael Camilleri ◽  
Russell B. Hanson ◽  
Donald E. Williams ◽  
Alfred J. Schei ◽  
...  
Keyword(s):  
Lower Esophageal Sphincter ◽  
Pain Perception ◽  
Motor Dysfunction ◽  
Gastric Distension ◽  
Gastric Accommodation ◽  
Standard Meal ◽  
Sphincter Function ◽  
Rumination Syndrome ◽  
Gastric Sensitivity ◽  
Esophageal Sphincter

Our hypothesis was that rumination syndrome is associated with gastric sensory and motor dysfunction. We studied gastric and somatic sensitivity, reflex relaxation of the lower esophageal sphincter (LES), and gastric compliance and accommodation postprandially and postglucagon. A barostatically controlled gastric bag and esophageal manometry were used to compare gastric sensorimotor functions and LES relaxation to gastric distension in 12 patients with rumination syndrome and 12 controls. During bag distensions, patients had greater nausea, bloating, and aggregate score, but not pain, compared with controls ( P < 0.05). At 4 and 8 mmHg gastric distension, LES tone reduction was greater in patients than in controls ( P < 0.05). Gastric compliance, accommodation to a standard meal, and response to glucagon were not different in patients and controls; however, 6 of 12 patients had no gastric accommodation; the latter patients had significantly greater pain perception during distension ( P < 0.05) but normal somatic sensitivity compared with healthy controls. Rumination syndrome is characterized by higher gastric sensitivity and LES relaxation during gastric distension. A subgroup of patients also had absent postprandial accommodation.

Inhibition of transient lower esophageal sphincter relaxations by electrical acupoint stimulation

2005 ◽  
Vol 289 (2) ◽  
pp. G197-G201 ◽  
Author(s):  
Duowu Zou ◽  
Wei Hao Chen ◽  
Katsuhiko Iwakiri ◽  
Rachael Rigda ◽  
Marcus Tippett ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Lower Esophageal Sphincter ◽  
Gastrointestinal Symptoms ◽  
Endogenous Opioids ◽  
Gastric Distension ◽  
Gastric Distention ◽  
Upper Gastrointestinal Symptoms ◽  
Esophageal Sphincter ◽  
And Function ◽  
Acupoint Stimulation

Acupuncture has been shown to modulate visceral sensation and function. Traditionally, stimulation at the Neiguan (pericardial meridian) has been used to treat upper gastrointestinal symptoms. Some of the effects of acupuncture may be mediated through release of endogenous opioids and are reversed by naloxone. Gastric distension is the major trigger for transient lower esophageal sphincter (LES) relaxations (TLESRs). The aim of this study was to investigate the effect of electric stimulation at the Neiguan and naloxone on the TLESRs. In 14 healthy volunteers, electrical acupoint stimulation was applied at the Neiguan and a sham point on the hip in randomized order on the same day. In 12 healthy volunteers, the effects of naloxone (80 μg/kg iv bolus injection) and saline on electrical acupoint stimulation were compared on separate days at least 1 wk apart. Esophageal motility was measured during distension of the proximal stomach with 500 ml of air using a barostat balloon. Electric acupoint stimulation at the Neiguan decreased the rate of TLESRs by ∼40% from a median of 6/h to 3.5/h ( P < 0.02). Acupoint stimulation had no effect on basal LES pressure, the residual LES pressure during TLESRs, the duration of TLESRs, or gastrointestinal symptoms of fullness, bloating, discomfort, or nausea. The effect of acupoint stimulation was not inhibited by naloxone. Electric acupoint stimulation at the Neiguan significantly inhibits the frequency of TLESRs in response to gastric distention in healthy subjects. This effect does not appear to be mediated through μ-opioid receptors.

Response of canine lower esophageal sphincter to gastric distension

1990 ◽  
Vol 259 (3) ◽  
pp. G380-G385 ◽  
Author(s):  
S. J. Franzi ◽  
C. J. Martin ◽  
M. R. Cox ◽  
J. Dent
Keyword(s):  
Lower Esophageal Sphincter ◽  
Gastric Wall ◽  
Progressive Increase ◽  
Truncal Vagotomy ◽  
Gastric Distension ◽  
Wall Tension ◽  
Proximal Stomach ◽  
Lower Esophageal Sphincter Relaxation ◽  
Esophageal Sphincter ◽  
Antral Distension

The aim of this study was to localize the region of the stomach responsible for triggering distension-induced transient lower esophageal sphincter relaxation (TLESR). The canine stomach was partitioned into subsegments by a row of buttressed sutures. This separated either the fundus from the lesser curve or the proximal stomach from the antrum. After 1 mo each region was progressively distended while gastroesophageal pressures were monitored. At the time of the first TLESR, gastric wall tension was estimated from the bag pressure and volume. Distension of the intact stomach, lesser curve, or proximal stomach in 12 dogs produced a progressive increase in lower esophageal sphincter (LES) pressure, which was interrupted at low gastric wall tension (29, 35, and 40 mmHg.cm, respectively) by a superimposed TLESR. Background LES pressure fell progressively with distension of the antrum but was unchanged by distension of the fundus alone. Both the fundus and antrum had significantly higher thresholds for triggering TLESR (96 and 105 mmHg.cm). In another two dogs truncal vagotomy performed at the time of gastric partitioning prevented both the change in background LES pressure, and the triggering of TLESR, associated with proximal gastric and antral distension. We conclude that the subcardiac region of the stomach is primarily responsible for triggering TLESR induced by distension and that the effect on background LES pressure depends on the region distended.

Effect of prolonged gastric distension on motor function of LES and of proximal stomach

2002 ◽  
Vol 283 (3) ◽  
pp. G677-G680 ◽  
Author(s):  
M. Allocca ◽  
M. Mangano ◽  
R. Penagini
Keyword(s):  
Lower Esophageal Sphincter ◽  
Motor Function ◽  
Healthy Subjects ◽  
Time Effect ◽  
Gastric Distension ◽  
Threshold Pressure ◽  
Proximal Stomach ◽  
Experimental Conditions ◽  
Esophageal Sphincter ◽  
Sensory Functions

Gastric distension is a potent stimulus of transient lower esophageal sphincter (LES) relaxation. To investigate the time effect of prolonged gastric distension on the rate of transient LES relaxations, LES pressure, and the motor and sensory functions of the proximal stomach, we performed a continuous isobaric distension of the proximal stomach at the 75% threshold pressure for discomfort for 2 h in seven healthy subjects. A multilumen assembly incorporating a sleeve and an electronic barostat was used. The rate of transient LES relaxations ( n/30 min) was constant during the first hour [4.1 ± 1.2 (0–30 min) and 5.4 ± 1.1 (30–60 min)] but markedly decreased ( P < 0.05) in the second hour [2.1 ± 0.5 (60–90 min) and 2.3 ± 0.9 (90–120 min)], whereas LES pressure, baseline volume and volume waves within the gastric bag, hunger, and fullness did not change throughout the experiment. It is concluded that the rate of transient LES relaxations decreases with time during prolonged gastric distension, thus suggesting that this type of stimulus should not be used in sequential experimental conditions.

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