Baclofen blocks LES relaxation and crural diaphragm inhibition by esophageal and gastric distension in cats

2002 ◽  
Vol 283 (6) ◽  
pp. G1276-G1281 ◽  
Author(s):  
Jianmin Liu ◽  
Nonko Pehlivanov ◽  
Ravinder K. Mittal
Keyword(s):  
Lower Esophageal Sphincter ◽  
Receptor Agonist ◽  
Gastric Distension ◽  
Emg Activity ◽  
Inhibitory Pathway ◽  
Surgical Implantation ◽  
Esophageal Sphincter ◽  
Adult Cats ◽  
Crural Diaphragm

Esophageal distension and transient lower esophageal sphincter (LES) relaxation (TLESR) are accompanied by simultaneous relaxation of the LES and inhibition of crural diaphragm. Recent studies indicate that baclofen decreases the frequency of TLESR; however, its effect on the crural diaphragm is not known. We evaluated the effects of baclofen on LES relaxation and crural diaphragm inhibition induced by gastric distension and esophageal distension in cats. Five adult cats underwent surgical implantation of wire electrodes into the crural and costal diaphragm for measurement of their EMG activity, respectively. One week after the surgery, animals were lightly sedated and recordings were performed using a manometry catheter equipped with a 2.5-cm balloon. The effects of baclofen (10 μmol/kg iv) on the graded esophageal distension and gastric distension-induced LES and crural diaphragm responses were studied. Distension of the esophagus and stomach induces relaxation of the LES and inhibition of the crural diaphragm, simultaneously. Baclofen blocks both the esophageal and the gastric distension-induced relaxation of the LES and inhibition of the crural diaphragm. The magnitude of response to baclofen was significantly larger for the crural diaphragm inhibition than for the LES relaxation. Baclofen, a GABABreceptor agonist, blocks the reflex inhibitory pathway to the LES and crural diaphragm. The reflex inhibitory pathway to the crural diaphragm is more sensitive to blockade by baclofen than the reflex LES inhibitory pathway.

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.

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.

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

Human lower esophageal sphincter pressure response to increased intra-abdominal pressure

1990 ◽  
Vol 258 (4) ◽  
pp. G624-G630 ◽  
Author(s):  
R. K. Mittal ◽  
M. Fisher ◽  
R. W. McCallum ◽  
D. F. Rochester ◽  
J. Dent ◽  
...  
Keyword(s):  
Lower Esophageal Sphincter ◽  
Esophagogastric Junction ◽  
Tonic Contraction ◽  
Pressure Response ◽  
Abdominal Pressure ◽  
Abdominal Compression ◽  
Gastric Pressure ◽  
Straight Leg Raising ◽  
Esophageal Sphincter ◽  
Crural Diaphragm

We studied the effects of increased intra-abdominal pressure on the lower esophageal sphincter (LES) pressure in 15 healthy subjects. The role of the diaphragm in the genesis of LES pressure during increased intra-abdominal pressure was determined by measuring diaphragm electromyogram (EMG). The latter was recorded using bipolar intraesophageal platinum electrodes that were placed on the nonpressure sensing surface of the sleeve device. We also measured the LES pressure response to increased intra-abdominal pressure during inhibition of the smooth muscles of the LES by intravenous atropine (12 micrograms/kg). Straight-leg raising and abdominal compression were used to increase intra-abdominal pressure. Our results show that the increase in LES pressure during straight-leg raising is greater than the increase in gastric pressure. During abdominal compression, the rate of LES pressure increase is faster than that of the gastric pressure, suggesting an active contraction at the esophagogastric junction. The increase in LES pressure during periods of increased intra-abdominal pressure is associated with a tonic contraction of the crural diaphragm as demonstrated by EMG recording. Atropine inhibited the resting LES pressure by 50-70% in each subject but had no effect either on the peak LES pressure attained during increased intra-abdominal pressure or tonic crural diaphragm EMG. We conclude that 1) there is an active contraction at the esophagogastric junction during periods of increased intra-abdominal pressure and 2) tonic contraction of the crural diaphragm is a mechanism for this LES pressure response.

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