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 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.

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.

Mechanoreceptors of the proximal stomach: Role in triggering transient lower esophageal sphincter relaxation

2004 ◽  
Vol 126 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Roberto Penagini ◽  
Stefania Carmagnola ◽  
Paolo Cantù ◽  
Mariangela Allocca ◽  
Paolo A. Bianchi
Keyword(s):  
Lower Esophageal Sphincter ◽  
Proximal Stomach ◽  
Lower Esophageal Sphincter Relaxation ◽  
Esophageal Sphincter

Transient Lower Esophageal Sphincter Relaxation in Morbid Obesity

2009 ◽  
Vol 19 (5) ◽  
pp. 595-600 ◽  
Author(s):  
J. H. Schneider ◽  
M. Küper ◽  
A. Königsrainer ◽  
B. Brücher
Keyword(s):  
Morbid Obesity ◽  
Lower Esophageal Sphincter ◽  
Lower Esophageal Sphincter Relaxation ◽  
Esophageal Sphincter

scholarly journals THE PARTICIPATION OF THE NITRERGIC PATHWAY IN INCREASED RATE OF TRANSITORY RELAXATION OF LOWER ESOPHAGEAL SPHINCTER INDUCED BY RECTAL DISTENSION IN DOGS

2014 ◽  
Vol 51 (2) ◽  
pp. 102-106 ◽  
Author(s):  
Michel Santos PALHETA ◽  
José Ronaldo Vasconcelos da GRAÇA ◽  
Armênio Aguiar dos SANTOS ◽  
Liziane Hermógenes LOPES ◽  
Raimundo Campos PALHETA JÚNIOR ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Lower Esophageal Sphincter ◽  
Esophageal Motility ◽  
Control Group ◽  
Rectal Distension ◽  
Evaluation Protocol ◽  
Lower Esophageal Sphincter Relaxation ◽  
Respective Control Group ◽  
Esophageal Sphincter ◽  
Pre Treatment

ContextThe rectal distension in dogs increases the rate of transitory lower esophageal sphincter relaxation considered the main factor causing gastroesophageal reflux.ObjectivesThe aim of this study was evaluate the participation of the nitrergic pathway in the increased transitory lower esophageal sphincter relaxation rate induced by rectal distension in anesthetized dogs.MethodsMale mongrel dogs (n = 21), weighing 10-15 kg, were fasted for 12 hours, with water ad libitum. Thereafter, they were anesthetized (ketamine 10 mg.Kg-1+ xylazine 20 mg.Kg-1), so as to carry out the esophageal motility evaluation protocol during 120 min. After a 30-minute basal period, the animals were randomly intravenous treated whith: saline solution 0.15M (1ml.Kg-1), L-NAME (3 mg.Kg-1), L-NAME (3 mg.Kg-1) + L-Arginine (200 mg.Kg-1), glibenclamide (1 mg.Kg-1) or methylene blue (3 mg.Kg-1). Forty-five min after these pre-treatments, the rectum was distended (rectal distension, 5 mL.Kg-1) or not (control) with a latex balloon, with changes in the esophageal motility recorded over 45 min. Data were analyzed using ANOVA followed by Student Newman-Keuls test.ResultsIn comparison to the respective control group, rectal distension induces an increase in transitory lower esophageal sphincter relaxation. Pre-treatment with L-NAME or methylene blue prevents (P<0.05) this phenomenon, which is reversible by L-Arginine plus L-NAME. However, pretreating with glibenclamide failed to abolish this process.ConclusionsTherefore, these experiments suggested, that rectal distension increases transitory lower esophageal sphincter relaxation in dogs via through nitrergic pathways.

Sign in / Sign up

Export Citation Format

Share Document