scholarly journals Experimental and Clinical studies on Lower Esophageal Sphincter Motor Function with special reference to the Influence of Vagal Denervation.

1994 ◽  
Vol 30 (3) ◽  
pp. 97-110 ◽  
Author(s):  
Sadanobu ABE
2001 ◽  
Vol 120 (5) ◽  
pp. A223-A223
Author(s):  
M VERKIJK ◽  
A HERTOG ◽  
C LAMERS ◽  
A MASCLEE

2001 ◽  
Vol 120 (5) ◽  
pp. A223
Author(s):  
M Verkijk ◽  
A.L. Hertog ◽  
C.B.H.W. Lamers ◽  
A.A.M. Masclee

2020 ◽  
Vol 22 (4) ◽  
pp. 37-42
Author(s):  
I. M. Pavlovich ◽  
G. A. Al’per ◽  
A. V. Gordienko ◽  
D. I. Proskunov ◽  
V. V. Yakovlev

The effect of morphological changes in the gastric mucosa on the motor-evacuation function of the stomach was evaluated in 90 patients with chronic atrophic gastritis and 93 patients with chronic non-atrophic gastritis aged 18 to 82 years. Motor function disturbances were discovered of 90% of patients with chronic atrophic gastritis and 80,6% with chronic non-atrophic gastritis. It was established that the pyloric insufficiency compared with its spasm was significantly more (p0,01) often in chronic atrophic gastritis. Insufficiency of the lower esophageal sphincter in patients with atrophic gastritis was significantly (p0,01). Insufficiency of the lower esophageal sphincter in combination with duodenogastric reflux in patients with chronic atrophic gastritis was significantly more (p0,01) often observed during diffuse atrophy, i. e. when mucous membrane of stomach corpus and antrum is involved in the process. With the localization of atrophy in the antrum alone, pyloric insufficiency was observed significantly more (p 0,01) often than spasm. Thus, an interrelation between the insufficiency of the lower esophageal and pyloric sphincters with the diffuse atrophic process has been established. There are no significant differences of disorders of gastric motor function in patients with different types of chronic gastritis. Accelerated evacuation from the stomach with localization of atrophy in the mucous membrane of the stomach corpus is more (p 0,01) often observed in patients with chronic atrophic gastritis.


1999 ◽  
Vol 135 (4) ◽  
pp. 517-521 ◽  
Author(s):  
Taher I. Omari ◽  
Marc A. Benninga ◽  
Christopher P. Barnett ◽  
Ross R. Haslam ◽  
Geoff P. Davidson ◽  
...  

2002 ◽  
Vol 283 (3) ◽  
pp. G677-G680 ◽  
Author(s):  
M. Allocca ◽  
M. Mangano ◽  
R. Penagini

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.


2000 ◽  
Vol 35 (11) ◽  
pp. 1666-1671 ◽  
Author(s):  
Hisayoshi Kawahara ◽  
Kenji Imura ◽  
Kiyokazu Nakajima ◽  
Makoto Yagi ◽  
Shinkichi Kamata ◽  
...  

1977 ◽  
Vol 232 (1) ◽  
pp. E19 ◽  
Author(s):  
A K Mukhopadhyay ◽  
N Weisbrodt

Intravenous administration of dopamine produced a dose-dependent decrease in lower esophageal sphincter pressure and a dose dependent increase in contractile activity of the body of the esophagus. The threshold dose of dopamine was 0.25 mug/kg, and the effect reached a plateau at about 6 mug/kg. A dose of 6 mug/kg of dopamine produced 83%+/-3 (SE) reduction in the lower esophageal sphincter pressure and 12+/-1 (SE) contractions in the body of the esophagus within 5 min of the bolus injection. Atropine, phentolamine, propranolol, and bilateral cervical vagotomy did not modify the effect of dopamine. Both haloperidol and bulbocapnine potently antagonized the effect of dopamine. The amplitude of esophageal contraction in the lower esophagus in response to pharyngeal stimulation and esiogageal distention was significantly increased after administration of haloperidol. It is concluded that intravenous administration of dopamine has potent effects on the motor function of the lower esophageal sphincter and the body of the esophagus. The effect of dopamine is not mediated via the vagal centers in the brain or cholinergic muscarinic and adrenergic receptors. The response of the smooth muscle segment of opossum esophagus to intravenous dopamine is mediated via specific dopamine receptors. The inhibitory dopamine receptors may play a physiological role in controlling the amplitude of esophageal contractions.


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