Sphincter Relaxations (sphincter + relaxation)

Distribution by Scientific Domains

Kinds of Sphincter Relaxations

  • lower oesophageal sphincter relaxation
  • oesophageal sphincter relaxation
  • transient lower oesophageal sphincter relaxation


  • Selected Abstracts


    Landmarks in the understanding and treatment of reflux disease

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2009
    John Dent
    Abstract The last 50 years have seen a transformation in the understanding and treatment of reflux disease. The development and wide use of flexible endoscopy and progressively more sophisticated approaches to measurement of pathophysiological factors have been major drivers of advances. The recognition and progressive elucidation of the mechanical events that comprise the transient lower esophageal sphincter relaxation and how they lead to reflux provide a novel and firm foundation for tailoring therapies that act directly to reduce occurrence of reflux episodes, either surgically or pharmacologically. Novel GABAB agonist drugs have been shown to inhibit transient relaxations and are currently being evaluated in clinical trials on patients with reflux disease. Better understanding has extended to recognition of the extraordinarily high prevalence of reflux disease and of the ability of proton pump inhibitor drugs to deliver major benefits to a high proportion of patients with reflux disease. The life of the Gastroenterological Society of Australia has spanned the period of these major advances. A large number of the members of the Society and their associates have contributed substantially to these advances. [source]


    Is aperistalsis with complete lower esophageal sphincter relaxation an early stage of classic achalasia?

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2007
    Jeong Hwan Kim
    Abstract Background:, Aperistalsis with complete lower esophageal sphinter (LES) relaxation, characterized by the complete relaxation of the LES and aperistalsis of the esophageal body on manometry, has been considered by some authors to be an early manifestation of classic achalasia, which is defined as incomplete relaxation of the LES and aperistalsis of the esophageal body. The aim of the present study was to compare the clinical features of patients with aperistalsis with complete LES relaxation, with those of patients with classic achalasia. Methods:, Eighteen patients with aperistalsis with complete LES relaxation and 53 patients with classic achalasia were analyzed with regard to clinical history, the maximal diameter of the esophageal body on barium esophagogram, LES resting pressure and the duration of LES relaxation on manometric recordings, and the selected treatment and its efficacy. Results:, The aperistalsis with complete LES relaxation group had distinctly different features compared to those of the classic achalasia group including older age, more frequent association with non-cardiac chest pain, less frequent association with dysphagia and weight loss, lower LES resting pressures, and longer duration of LES relaxation. However, the two groups were similar in terms of maximal diameter of the esophageal body, and efficacy associated with pneumatic dilation. Conclusions:, Aperistalsis with complete LES relaxation on manometry is not necessarily an early manifestation of classic achalasia. However, this condition does not preclude a diagnosis of achalasia or a good response to achalasia therapy. [source]


    Lower oesophageal sphincter relaxation evoked by stimulation of the dorsal motor nucleus of the vagus in ferrets

    NEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2002
    T. P. Abrahams
    Abstract, An understanding of the neural control of lower oesophageal sphincter (LOS) relaxation is clinically relevant because transient LOS relaxations (TLOSRs) are a mechanism of acid reflux into the oesophagus. Preganglionic motor neurones innervating the LOS are localized in the dorsal motor nucleus of the vagus (DMV). Based on a single study in cats, it is now widely accepted that these neurones are functionally organized into two separate populations, such that stimulation of the caudal and rostral DMV evokes LOS relaxation and contraction, respectively. Our goal was to map the functional LOS responses to chemical stimulation in the DMV and nucleus tractus solitarius (NTS) of ferrets, an animal model commonly used for conscious studies on TLOSRs, and to test whether DMV-evoked LOS relaxation is mediated through hexamethonium-sensitive vagal-inhibitory pathways to the LOS. We used miniaturized manometry with Dentsleeve to monitor LOS and oesophageal pressures in decerebrate unanaesthetized ferrets. LOS relaxation was evoked readily in response to gastric insufflation, which shows that the vago,vagal reflex was intact in this preparation. Microinjections of l -glutamate (12.5 nmol L,1in 25 nL) were made into the DMV from approximately ,,1.5 to +,2.0 mm relative to the obex. Microinjections into the caudal (, 1.5 to +,0.0 mm behind obex) and intermediate (+ 0.1 to +,1.0 mm rostral to obex) DMV both significantly decreased LOS pressure, and complete LOS relaxation was noted in 28/32 and 11/18 cases, respectively. LOS relaxation responses to DMV microinjection were highly reproducible and abolished by bilateral vagotomy or hexamethonium (15 mg kg,1intravenously). A nitric oxide synthase inhibitor (l -NAME 100 mg kg,1intramuscularly) significantly increased the time taken to reach the maximal response. Increases in LOS pressure (24 ± 4 mmHg; n = 3) were obtained only when stimulation sites were located equal to greater than 1.5 mm rostral to the obex. LOS relaxation (, 78 ± 10%; n = 6) was evoked by stimulation of the NTS but not immediately outside of the NTS (11 ± 27%; n = 5). We conclude that there is a very extensive population of ,inhibitory' motor neurones in the DMV that may account for the predominant vagal-inhibitory tone in ferrets. As NTS stimulation evokes LOS relaxation and the predominant response to DMV stimulation is also LOS relaxation, this vago,vagal reflex may involve an excitatory interneurone between the NTS and DMV vagal inhibitory output. [source]


    Videomanofluorometric Study in Amyotrophic Lateral Sclerosis

    THE LARYNGOSCOPE, Issue 5 2002
    Ryuzaburo Higo MD
    Abstract Objective To elucidate the time-course changes of swallowing function in amyotrophic lateral sclerosis (ALS) by videomanofluorometry. Study Design Videomanofluorometry was conducted on 21 patients with ALS, who were divided into five groups according to type of disease and according to the length of time following the appearance of bulbar symptoms. Methods Videomanofluorometry, which is videofluoroscopic and manometric study conducted simultaneously, was performed on patients in the five groups, and swallowing function in each group was evaluated. Some of the patients were followed up by videomanofluorometry performed several times, and their swallowing function changes over time were investigated. Results A decrease of swallowing pressure first appeared in the oropharynx, then the hypopharynx became involved. Oropharyngeal swallowing pressure had already decreased to approximately 50 mm Hg within 6 months after the appearance of bulbar symptoms; however, hypopharyngeal swallowing pressure was relatively maintained until 1 year after the onset of bulbar symptoms. Most of the patients with ALS maintained normal upper esophageal sphincter relaxation, but upper esophageal sphincter spasm was seen in some patients with ALS. Aspiration was seen in eight cases, five of which showed upper esophageal sphincter spasm. Conclusions Patients with ALS gradually face the danger of aspiration as decreases of oropharyngeal and hypopharyngeal swallowing pressure progress. Upper esophageal sphincter spasm occurs in some patients with ALS, and it is an important cause of aspiration. Both videofluoroscopic and manometric evaluation are necessary to assess these conditions, and they are quite useful for follow-up of swallowing function in patients with ALS. [source]


    Effects of acute hyperglycaemia on anorectal motor and sensory function in diabetes mellitus

    DIABETIC MEDICINE, Issue 2 2004
    A. Russo
    Abstract Aims To determine the effects of acute hyperglycaemia on anorectal motor and sensory function in patients with diabetes mellitus. Methods In eight patients with Type 1, and 10 patients with Type 2 diabetes anorectal motility and sensation were evaluated on separate days while the blood glucose concentration was stabilized at either 5 mmol/l or 12 mmol/l using a glucose clamp technique. Eight healthy subjects were studied under euglycaemic conditions. Anorectal motor and sensory function was evaluated using a sleeve/sidehole catheter, incorporating a barostat bag. Results In diabetic subjects hyperglycaemia was associated with reductions in maximal (P < 0.05) and plateau (P < 0.05) anal squeeze pressures and the rectal pressure/volume relationship (compliance) during barostat distension (P < 0.01). Hyperglycaemia had no effect on the perception of rectal distension. Apart from a reduction in rectal compliance (P < 0.01) and a trend (P = 0.06) for an increased number of spontaneous anal sphincter relaxations, there were no differences between the patients studied during euglycaemia when compared with healthy subjects. Conclusions In patients with diabetes, acute hyperglycaemia inhibits external anal sphincter function and decreases rectal compliance, potentially increasing the risk of faecal incontinence. Diabet. Med. 21, 176,182 (2004) [source]


    Effect of lesogaberan, a novel GABAB -receptor agonist, on transient lower oesophageal sphincter relaxations in male subjects

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 11 2010
    G. E. BOECKXSTAENS
    Aliment Pharmacol Ther,31, 1208,1217 Summary Background, Transient lower oesophageal sphincter relaxations (TLESRs) are a major mechanism behind gastro-oesophageal reflux disease (GERD). Aim, To assess the effect of lesogaberan (AZD3355) , a novel peripherally active GABAB receptor agonist , on TLESRs. Methods, Twenty-four healthy men were enrolled in this single-blind, placebo-controlled, randomized, single-centre, three-period crossover phase 1 study. Subjects were randomized to receive single oral doses of lesogaberan (0.8 mg/kg), baclofen (40 mg) and placebo, separated by washout periods of ,7 days. Subjects finished a meal 1 h after the dose. Oesophageal manometry and pH-metry measurements were taken during the 3 h after the meal. Results, Twenty-one subjects completed the study. Compared with placebo, lesogaberan 0.8 mg/kg significantly reduced the number of TLESRs by 36% [geometric mean ratio (GMR): 0.64; 95% confidence interval (CI): 0.51,0.82] and significantly reduced the number of acid reflux episodes (mean reduction: 1.6; 95% CI: 0.34,2.9). Lesogaberan also significantly increased lower oesophageal sphincter (LES) pressure by 39% compared with placebo (GMR: 1.39; 95% CI: 1.18,1.64). Comparable results were observed with baclofen. Similar numbers of adverse events were reported by subjects taking lesogaberan and placebo. Conclusion, Compared with placebo, lesogaberan significantly reduced TLESRs and acid reflux episodes and increased LES pressure. [source]


    The GABAB receptor agonist AZD9343 inhibits transient lower oesophageal sphincter relaxations and acid reflux in healthy volunteers: a phase I study

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2009
    H. BEAUMONT
    Summary Background, Transient lower oesophageal sphincter relaxations (TLESRs) represent an interesting target for the treatment of gastro-oesophageal reflux. Baclofen reduces TLESRs and reflux episodes, but is not optimal for clinical application because of its central side effects. Therefore, new agents are required. Aim, To study the effect of AZD9343, a new selective GABAB receptor agonist, in healthy volunteers. Methods, A total of 27 subjects participated in a placebo-controlled, randomized, two-centre phase I study. Subjects underwent oesophageal manometry and pH-metry for 3 h postprandially. Before meal ingestion, a single oral dose of placebo, 60 and 320 mg AZD9343 or 40 mg baclofen was given on four separate days. Results, Somnolence was reported after 320 mg AZD9343 and baclofen. Reversible short-lasting paraesthesia was reported after AZD9343. AZD9343 320 mg and baclofen significantly reduced the number of TLESRs with 32% and 40% respectively. Acid reflux was significantly decreased by AZD9343 and baclofen. Like baclofen, AZD9343 increased LES pressure before meal intake. AZD9343 320 mg and baclofen significantly reduced the swallowing rate. Conclusions, Like baclofen, AZD9343 dose-dependently decreases the number of TLESRs and acid reflux episodes, increases LES pressure and reduces swallowing, extending the concept that GABAB agonists are potent reflux inhibitors. However, discovery of analogues with an improved side effect profile is warranted. [source]


    The effect of baclofen on gastro-oesophageal reflux, lower oesophageal sphincter function and reflux symptoms in patients with reflux disease

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2002
    M. A. Van Herwaarden
    SUMMARY Background :,Baclofen decreases gastro-oesophageal reflux episodes in healthy subjects by reducing the incidence of transient lower oesophageal sphincter relaxations. Aim :,To investigate the effect of baclofen on reflux symptoms, oesophageal pH and lower oesophageal sphincter manometry in patients with gastro-oesophageal reflux disease. Methods :,A double-blind, placebo-controlled, two-way crossover design was used to study the effect of baclofen on heartburn and regurgitation 3 h after a provocation test meal in 37 patients with gastro-oesophageal reflux disease. Additionally, in 20 of these patients, the effect of baclofen on oesophageal pH, transient lower oesophageal sphincter relaxations and basal lower oesophageal sphincter pressure was studied. Results :,Baclofen significantly decreased the acid reflux time and the incidence of gastro-oesophageal reflux episodes (8.3 ± 8.8% vs. 12.4 ± 12.0%, P = 0.03 and 10.9 ± 7.3 per 3 h vs. 18.7 ± 12.4 per 3 h). The incidence of transient lower oesophageal sphincter relaxations was significantly lower with baclofen than with placebo (15.1 ± 6.4 per 3 h vs. 22.8 ± 5.4 per 3 h, P < 0.0001). Lower oesophageal sphincter pressure and the percentage of transient lower oesophageal sphincter relaxations associated with reflux were not affected by baclofen. No significant effect on symptom scores was observed. Conclusions :,Baclofen decreases post-prandial acid reflux in patients with gastro-oesophageal reflux disease by reducing the incidence of transient lower oesophageal sphincter relaxations. No effect of a single dose of baclofen on reflux symptoms could be demonstrated in this 3-h post-prandial study. [source]


    The effect of glucagon-induced gastric relaxation on TLOSR frequency

    NEUROGASTROENTEROLOGY & MOTILITY, Issue 1 2003
    H. Y. Chang
    Abstract This study aimed to determine the effect of glucagon-induced gastric relaxation on the frequency of transient lower oesophageal sphincter relaxations (TLOSRs). Eight normal subjects (four male, age 18,52 y) were studied after a 6-h fast using a combined manometric barostat assembly. The recording was divided into two 1-h sessions: (1) a baseline period with the barostat set at minimal distending pressure (MDP) + 2 mmHg and (2) a period with continuous glucagon or placebo infusion with barostat set at MDP + 2 mmHg. Patients were studied on two different days and randomly received glucagon (4.8 ,g kg,1 bolus followed by 9.6 ,g kg,1 h,1 infusion) on 1 day and placebo (saline) on another. Lower oesophageal sphincter (LOS) pressure, frequency of TLOSRs, and barostat bag volumes were determined for both placebo and glucagon infusion. Glucagon induced significant fundal relaxation compared with placebo (P < 0.05) and significantly decreased baseline LEOS pressure (P < 0.05). The frequency of TLOSRs was not altered by glucagon infusion compared with placebo. Despite causing substantial proximal stomach relaxation, glucagon did not increase TLOSR frequency. This suggests that the relevant gastric mechanoreceptors responsible for triggering TLOSRs do not respond to passive elongation. [source]