Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ERUCTATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1986

Abolition of gas reflux and transient lower esophageal sphincter relaxation by vagal blockade in the dog.

In the present study we have examined the hypothesis that transient lower esophageal sphincter relaxations are under vagal control. Fasting esophageal motor function was monitored with a manometric sleeve catheter passed via a cervical esophagostomy. Gastric insufflation with oxygen resulted in intermittent venting of gas into the esophagus during transient lower esophageal sphincter relaxations. Such venting of gas was associated with the occurrence of esophageal body common cavities and gas venting from the esophageal stoma, all of which increased with increasing rates of gastric insufflation. The optimal insufflation rate, 80 ml/min, produced stomal gas venting at a rate of 10.3 +/- 1.1/h (mean +/- SE). The time and pressure profiles of transient lower esophageal sphincter relaxations induced by gastric insufflation were similar to those relaxations seen with spontaneous postprandial gastroesophageal reflux and belching in dogs. Sphincteric relaxation started 10 s before the onset of common cavities. In all 4 dogs, cooling of cervical subcutaneous vagosympathetic loops abolished transient lower esophageal sphincter relaxations, common cavities, and stomal gas venting. Within 1-4 min of cessation of vagal cooling, all three markers of gastroesophageal gas venting returned. Atropine, 50 and 200 micrograms/kg i.v., did not block transient lower esophageal sphincter relaxations or gas reflux. Gastric gaseous distention is a potent and consistent trigger of transient lower esophageal sphincter relaxations in the dog. This effect can be used as a model for study of control mechanisms of transient sphincter relaxation-dependent gastroesophageal reflux. Our observations with this model indicate that transient lower esophageal sphincter relaxations are under vagosympathetic control, but that muscarinic mechanisms are not important mediators of this control.

Animals↗
PubMed1986

Relationship of transient lower esophageal sphincter relaxation to postprandial gastroesophageal reflux and belching in dogs.

Methods have been developed for the recording of patterns of motor function associated with spontaneous gastroesophageal reflux and belching in trained, unsedated dogs. Pharyngeal, esophageal body, lower esophageal sphincter (LES), and gastric pressures were monitored in 3 dogs with a manometric assembly inserted through a cervical esophagostomy. Spontaneous changes in esophageal pH were recorded simultaneously with a glass electrode. Each dog was studied three times for 3 h starting directly after completion of a full-sized meal. Acid reflux was recorded on 40 occasions; on 35 of these occasions it was possible to analyze, in detail, motor events at the time of reflux. This analysis showed that the LES was completely relaxed at the time of reflux and that the relaxation occurred within the 15 s before the onset of esophageal acidification. In 77% of the reflux episodes LES relaxation occurred independently of swallowing or any other motor event. The remainder of the LES relaxations associated with reflux were secondary to a swallowing salvo or a single swallow that did not trigger an esophageal body peristaltic wave. Straining was associated with reflux during many episodes of LES relaxation, but did not induce reflux if there was measurable LES pressure. Belching was also related to complete LES relaxations with a pattern identical to that associated with acid reflux. In the dog, liquid and gas reflux occurred during transient LES relaxations that were very similar to those that allow reflux to occur in humans. The dog is a suitable model for investigation of the nature and control of reflux associated with transient LES relaxation.

Animals↗
PubMed1987

Dysfunction of the belch reflex. A cause of incapacitating chest pain.

We report a 25-yr-old woman who suffered incapacitating chest pain caused by upper esophageal sphincter (UES) dysfunction. She presented with a long history of severe episodic chest pain associated with gurgling noises in her chest and was unable to belch despite feeling a need to do so during pain episodes. Fluoroscopic and manometric studies confirmed that the patient's chest pain and gurgling noise were associated with dysfunction of the belch reflex. Although reflux of gas from the stomach into the esophageal body occurred normally, the extreme esophageal distention resulting from the gas reflux failed to trigger UES relaxation. Consequently, there was no venting of gas across the UES. The gurgling noise was caused by the gastroesophageal reflux of gas and the pain was associated with profound esophageal distention. A manometric study of the UES revealed absent or incomplete UES relaxation in response to abrupt esophageal distention by gastroesophageal gas reflux, so that the nadir of UES pressure always exceeded esophageal body pressure. The distended esophagus was repeatedly cleared by secondary peristalsis. To our knowledge this is the first description of chest pain caused by dysfunction of the belch reflex. We speculate that the mechanism described in this patient may account for a subgroup of patients with "chest pain of esophageal origin."

Adult↗
PubMed1989

Acute airway obstruction in achalasia. Possible role of defective belch reflex.

Achalasia presenting as an acute airway obstruction is a rarely reported phenomenon. The pathophysiology of this dramatic complication of achalasia remains an enigma. Our patient with achalasia presented with an acute airway compromise necessitating emergent endotracheal intubation. We review the available literature on this interesting yet rare complication of achalasia. We also add some information to help elucidate the possible pathophysiologic mechanism of this emergency, proposing that specific upper esophageal sphincter manometry may indicate abnormality of the "belch reflex."

Airway Obstruction↗
PubMed1992

Alteration of the upper esophageal sphincter belch reflex in patients with achalasia.

Some patients with achalasia have been reported to develop airway obstruction from a massively air-distended esophagus, which may represent an abnormality in the upper esophageal sphincter belch reflex. When questioned carefully, 95% of our achalasia patients reported difficulty with belching. The upper esophageal belch reflex in 23 consecutive achalasia patients and 12 healthy controls was studied using an upper esophageal sphincter sleeve manometry catheter and rapid injection of 20-50 mL of air into the midesophagus. Compared with normal subjects, achalasia patients were significantly less likely to have an esophageal belch for all volumes tested and were more likely to have an increase rather than a decrease in upper esophageal sphincter pressure in response to air injection. This study systematically documents that many achalasia patients have an alteration in the upper esophageal sphincter belch reflex that may be a contributory mechanism for some of the chest and upper airway symptoms reported by some patients during acute esophageal distension.

Adolescent↗
PubMed1991

Belching.

Explore the source record for details and available documents.

Diagnosis, Differential↗
PubMed1992

High-frequency diaphragmatic flutter: symptoms and treatment by carbamazepine.

Classic diaphragmatic flutter, a rare disorder associated with dyspnoea, thoracic or abdominal wall pain, and epigastric pulsations, is caused by involuntary contractions of the diaphragm with a frequency of 0.5-8.0 Hz. We have seen three patients with diaphragmatic flutter of higher frequency not associated with respiratory disease. The patients presented with longstanding oesophageal belching, hiccups, and retching, respectively. The diagnosis was established by the presence on electromyography of the diaphragm and scalene and parasternal intercostal muscles of repetitive discharges of 9-15 Hz. Spirographic tracings, especially those of volume or flow vs time, showed similar high-frequency oscillations superimposed on tidal respiratory movements. Treatment with carbamazepine 200-400 mg three times daily led to disappearance or great improvement of flutter and clinical symptoms in all three patients. The phenomenon was not seen in other patients with chronic hiccups or oesophageal belching or in patients without these symptoms who had undergone electromyography or spirography for other reasons. Thus, high-frequency diaphragmatic flutter seems to be a new disease entity. The response to carbamazepine, which suggests that the flutter causes the symptoms, requires further study.

Adult↗
PubMed2004

Pathophysiology of functional dyspepsia.

Functional dyspepsia is a highly prevalent symptom complex and a heterogeneous disorder. Recent studies showed potential associations between specific pathophysiologic disturbances and dyspeptic symptoms. Delayed gastric emptying reported in about 30% of patients with functional dyspepsia is associated with the symptoms of postprandial fullness, nausea, and vomiting. Impaired gastric accommodation present in 40% of functional dyspepsia patients is found to be associated with early satiety. Hypersensitivity to gastric distension is observed in 37% of functional dyspepsia patients and associated with the symptoms of postprandial pain, belching, and weight loss. Psychosocial factors and altered response to duodenal lipids or acid have also been identified as pathophysiologic mechanisms.

Dyspepsia↗
PubMed2006

Assessment of diaphragmatic stressors as risk factors for symptomatic failure of laparoscopic nissen fundoplication.

An important limitation of antireflux surgery is a 5%-10% failure rate. We investigated the correlation between various diaphragm stressors and failure of antireflux surgery. Forty-one study cases who underwent a reoperative antireflux operation from 1997 to 2001 and 50 control patients who had undergone a successful laparoscopic Nissen fundoplication during the same period without clinical or symptomatic evidence of failure were randomly selected for comparison. A retrospective analysis was conducted utilizing a standardized diaphragm stressor questionnaire, addressing the period between the primary and secondary operation. Stressors considered in the study included height, body mass index (BMI), postoperative gagging, vomiting, weight lifting (greater than 100 pounds), coughing, hiccuping, motion sickness, retching, belching, antidepressant use, smoking, preoperative grade of esophagitis, size of hiatal hernia, lower esophageal sphincter pressure, esophageal body pressures, and preoperative response to proton pump inhibitors. Of the potential stressors investigated, the following were significantly associated with surgical failure after adjusting for other variables through multivariate analysis: gagging (P = 0.005), belching (P = 0.02), and hernia size greater than 3 cm (P = 0.04; Table 1). Other potential risk factors show trends as obvious in Fig. 2. Vomiting was significant (P = 0.01) in the earlier models but lost significance when logistic regression was applied. Patients with postoperative gagging and an intraoperative hiatal hernia (greater than 3 cm) have a poorer outcome, whereas patients with postoperative belching have a better long-term outcome.

Adolescent↗
PubMed2006

Inappropriate mediastinal baroreceptor reflex as a possible cause of sudden infant death syndrome - Is thorough burping before sleep protective?

Despite extensive research, a link between the assumed mechanisms of death and known risk factors for sudden infant death syndrome (SIDS) has not yet been established. Modifiable risk factors such as prone sleeping position, nicotine exposure and thermal stress and non-avoidable risk factors like male gender and some risky socio-economic conditions could be detected, but the etiology of SIDS remains unknown. In many SIDS cases histopathological findings suggest an involvement of vital autonomic control functions and unidentified trigger factors seem to play a role. From a hypothetical point of view, a developmental sympatheticovagal imbalance of the cardiovascular reflex control could cause a predisposition for SIDS. An assumed gastroesophageal trigger impulse is possibly developed during the first weeks of life and could lead to the infant's vagal reflex death. Air swallowed during feeding escapes through the esophagus while the infant is sleeping. The temporarily bloated esophagus exerts pressure on neighboring mediastinal baroreceptors, which is potentially misinterpreted as a rise in arterial pressure. The following cardiodepressoric baroreceptor reflex could lead to arterial hypotension, bradycardia and cardiac arrest. Sleeping in prone position may create an increased thoracic pressure on mediastinal baroreceptors, causing a more pronounced vagal reflex and an increased likelihood of SIDS. Prone position in connection with soft objects in the infant's sleeping environment potentially generates an increased oculobulbar pressure, resulting in an additional cardiodepressoric condition (Aschner-Dagnini phenomenon). From the sixth month of life onwards the sympatheticovagal balance seems to have matured sufficiently to compensate the life-threatening challenges in most infants. Insufficient postprandial burping could either create another independent modifiable risk factor or present the missing link to a common trigger mechanism for SIDS. Further investigations may possibly lead to the explicit recommendation to burp all infants sufficiently and repeatedly before sleep.

Baroreflex↗
PubMed1998

[Functional results of the laparoscopic treatment of gastroesophageal reflux (followup greater than 2 years)].

STUDY AIM: The of this study was to evaluate functional results in 70 patients operated on for gastroesophageal reflux disease with a follow-up > 2 years, by means of a questionnaire sent to them. PATIENTS AND METHODS: Functional results were evaluated in the 60 patients who answered the questionnaire. The fundoplication (Nissen = 27, Nissen-Rosseti = 21, Toupet (n = 12) was laparoscopically performed with a mean follow-up of 3.4 years (range: 2-6.6 years). A circular wrap (either Nissen or Nissen-Rossetti) had been systematically performed except in patients who had an esophageal motility disorder, who had a partial wrap according to Toupet. RESULTS: Three patients experienced recurrent symptoms of reflux (failure rate: 5%). Thirteen patients had mild dysphagia, requiring modification of the oral intake in two cases. No patient required dilatation. Fifty patients complained of postoperative side effects: flatulence (n = 40), meteorism (n = 24), abdominal pain (n = 16), diarrhea (n = 12), impossibility either to vomit (n = 16) or to belch (n = 20). Ten patients were symptom free and had neither symptoms of reflux nor side effects. Despite undesirable side effects, 46 patients (78%) were very satisfied with the operation, six (10%) were satisfied and five (8%) were disappointed. CONCLUSION: Recurrent symptoms of reflux were rarely observed (5%) but postoperative side effects were frequent (67%). Side effects when present provide less discomfort than reflux itself. Patients must be aware of it prior to surgery. These results should be confirmed by further assessments.

Abdominal Pain↗
PubMed1997

Upper esophageal sphincter function during antegrade and retrograde transit.

The striated musculature of the UES, along with the cricoid and thyroid cartilages, the hyoid bone, their ligaments, and the supra- and infrahyoid musculature form a functional unit that selectively controls the opening and closing of the esophageal inlet. At rest, upper esophageal tone acts as a barrier against both entry of air into the esophagus and regurgitation of materials coming from the proximal esophagus. However, reflexive responses of the sphincter offer no substantial protection against regurgitation of stomach contents that cause substantial esophageal distension. Although esophageal distention can experimentally induce sphincter contraction, this potential protective reflex against esophago-pharyngeal reflux has not been observed during spontaneous gastroesophageal reflux episodes. Furthermore, owing to the effects of gaseous distention, regurgitation may be more likely when acid and gaseous contents gastroesophageal reflux together. Modulation of the timing and the extent of sphincter opening during swallowing is intimately correlated with the volume and physical properties of the bolus, along with coordinated activity of the tongue, pharyngeal constrictors, and hyoid musculature, which suggests continuous sensory feedback throughout the pharyngeal swallow.

Animals↗