Esophageal responses to transient and sustained esophageal distension

Wg, Paterson; Rattan, Satish; Goyal, Raj K.

doi:10.1152/ajpgi.1988.255.5.g587

Cited by 24 publications

(25 citation statements)

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“…It is apparent from liter ature data that the duration, volume and site of esophage al distension may determine whether the response will be propagated or simultaneous. Prolonged balloon disten sions provoked nonperistaltic contractions upon balloon deflation [10,15,16]; the more proximal the distension, the more likely it became that the response was propa gated [17].…”

Section: Discussionmentioning

confidence: 99%

Secondary Peristaltic Contractions, like Primary Peristalsis, Are Preceded by Inhibition in the Human Esophageal Body

Sifrim¹,

Janssens²

1996

Digestion

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Swallow-induced esophageal peristalsis is preceded by a wave of inhibition in the esophageal body. The aim of this study was to determine whether a similar wave of inhibition precedes secondary peristalsis. Primary and secondary peristalsis were studied in 6 healthy subjects. Inhibition was visualized as relaxation of an artificial high-pressure zone which was created in the esophageal body by the inflation of a small intraesophageal balloon. Secondary peristaltic contractions induced by injection of 10 ml of air in the proximal esophagus or secondary peristaltic contractions spontaneously occurring after repeated swallowing were preceded by inhibition similar to that observed in primary peristalsis (96.4 ± 2.8%, 93.2 ± 4.2% and 91.5 ± 3.3%) respectively. It is concluded that physiologically triggered secondary peristaltic contractions are preceded by inhibition in the esophageal body.

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Section: Discussionmentioning

confidence: 99%

Secondary Peristaltic Contractions, like Primary Peristalsis, Are Preceded by Inhibition in the Human Esophageal Body

Sifrim¹,

Janssens²

1996

Digestion

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“…In the current study, esophageal striated muscle peristaltic waves started when acidic infusate reached the cervical esophagus and was repeatedly generated every 5–6 seconds till cessation of slow acid infusion. Rhythmic isolated striated segment peristaltic activity in the absence of distal esophageal smooth muscle peristalsis during slow esophageal liquid distention, may represent inhibition of smooth muscle activity resembling distal esophageal quiescence observed during sustained balloon distention in animal models 16 . On the other hand, delayed esophageal non-peristaltic contractions seen in GERD and SERD patients could be associated with “esophageal stasis” related distention, comparable to myogenic esophageal non-peristaltic contractions reported during sustained balloon distention 15, 16 .…”

Section: Discussionmentioning

confidence: 98%

“…EUCR and esophageal contractile response are both mediated through esophageal slowly adapting mechanoreceptors believed to reside within the muscularis propria 14 . Animal studies have shown that EUCR and proximal esophageal contractile response above an esophageal distending balloon are vagally mediated and cholinergically dependent 14, 15 , while phasic esophageal contractile response at the site of balloon distention and distally is preserved even after vagotomy and is not sensitive to cholinergic blockade 15, 16 . Based on the observation that the UES was able to mount a response more frequently when greater sensory stimulus of rapid saline injection (compared to slow) was applied; and based on presence of delayed but normal amplitude UES and esophageal contractile response in patients we speculate that the observed differences between healthy controls, GERD and SERD patients could be in part due to graded dysfunction of the afferent arm of the esophageal and UES reflexes.…”

Section: Discussionmentioning

confidence: 99%

Impaired Upper Esophageal Sphincter Reflexes in Patients With Supraesophageal Reflux Disease

et al. 2015

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Background & Aims Normal responses of the upper esophageal sphincter (UES) and esophageal body to liquid reflux events prevent esophagopharyngeal reflux and its complications, but abnormal responses have not been characterized. We investigated whether patients with supra-esophageal reflux disease (SERD) have impaired UES and esophageal body responses to simulated reflux events. Methods We performed a prospective study of 25 patients with SERD (19–82 y old, 13 female) and complaints of regurgitation and supra-esophageal manifestations of reflux. We also included 10 patients with gastroesophageal reflux disease (GERD; 32–60 y old, 7 female) without troublesome regurgitation and supra-esophageal symptoms and 24 healthy asymptomatic individuals (controls; 19–49 y old, 13 female). UES and esophageal body pressure responses, along with luminal distribution of infusate during esophageal rapid and slow infusion of air or liquid, were monitored by concurrent high-resolution manometry and intraluminal impedance. Results A significantly smaller proportion of patients with SERD had UES contractile reflexes in response to slow esophageal infusion of acid than controls or patients with GERD. Only patients with SERD had abnormal UES relaxation responses to rapid distension with saline. Diminished esophageal peristaltic contractions resulted in esophageal stasis in patients with GERD or SERD. Conclusions Patients with SERD and complaints of regurgitation have impaired UES and esophageal responses to simulated liquid reflux events. These patterns could predispose them to esophagopharyngeal reflux.

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“…Human and animal studies show that LES relaxation associated with swallow (3), balloon distension of the esophagus (19), and electrical stimulation of the vagus nerve (4) is associated with cranial displacement of the LES. The latter is the result of the contraction of the longitudinal muscle layer of the esophagus.…”

Section: Discussionmentioning

confidence: 99%

Variability in the muscle composition of rat esophagus and neural pathway of lower esophageal sphincter relaxation

Jiang

Bhargava

Lal

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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Jiang Y, Bhargava V, Lal HA, Mittal RK. Variability in the muscle composition of rat esophagus and neural pathway of lower esophageal sphincter relaxation. Am J Physiol Gastrointest Liver Physiol 301: G1014 -G1019, 2011. First published September 1, 2011; doi:10.1152/ajpgi.00273.2011.-Several studies from our laboratory show that axial stretch of the lower esophageal sphincter (LES) in an oral direction causes neurally mediated LES relaxation. Under physiological conditions, axial stretch of the LES is caused by longitudinal muscle contraction (LMC) of the esophagus. Because longitudinal muscle is composed of skeletal muscle in mice, vagalinduced LMC and LES relaxation are both blocked by pancuronium. We conducted studies in rats (thought to have skeletal muscle esophagus) to determine if vagus nerve-mediated LES relaxation is also blocked by pancuronium. LMC-mediated axial stretch on the LES was monitored using piezoelectric crystals. LES and esophageal pressures were monitored with a 2.5-Fr solid-state pressure transducer catheter. Following bilateral cervical vagotomy, the vagus nerve was stimulated electrically. LES, along with the esophagus, was harvested after in vivo experiments and immunostained for smooth muscle (smooth muscle ␣-actin) and skeletal muscle (fast myosin heavy chain). Vagus nerve-stimulated LES relaxation and esophageal LMC were reduced in a dose-dependent fashion and completely abolished by pancuronium (96 g/kg) in six rats (group 1). On the other hand, in seven rats, LES relaxation and LMC were only blocked completely by a combination of pancuronium (group 2) and hexamethonium. Immunostaining revealed that the longitudinal muscle layer was composed of predominantly skeletal muscle in the group 1 rats. On the other hand, the longitudinal muscle layer of group 2 rats contained a significant amount of smooth muscle (P Ͻ 0.05). Our study shows tight coupling between axial stretch on the LES and relaxation of the LES, which suggests a cause and effect relationship between the two. We propose that the vagus nerve fibers that cause LMC induce LES relaxation through the stretch-sensitive activation of inhibitory motor neurons. vagl pathway to lower esophageal sphincter; inhibitory motor neurons of lower esophageal sphincter; longitudinal muscle esophagus THE LOWER ESOPHAGEAL SPHINCTER (LES) guards entrance of the esophagus into the stomach. The LES works like a "two-way valve"; it allows passage of esophageal contents into the stomach with swallow (swallow-induced LES relaxation) and passage of gastric contents into the esophagus with belching and vomiting (transient LES relaxation) (14). Inadequate LES relaxation leads to achalasia and possibly other esophageal motor disorders (16) and LES incompetence (too much relaxation) leading to gastroesophageal reflux (15). Complications of reflux disease, i.e., esophagitis, strictures, angina-like pain, and extraesophageal symptoms related to the ear, nose, throat, larynx, and respiratory tract, are the leading causes of medical morbidity. Therefore, an...

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Esophageal responses to transient and sustained esophageal distension

Cited by 24 publications

References 0 publications

Secondary Peristaltic Contractions, like Primary Peristalsis, Are Preceded by Inhibition in the Human Esophageal Body

Secondary Peristaltic Contractions, like Primary Peristalsis, Are Preceded by Inhibition in the Human Esophageal Body

Impaired Upper Esophageal Sphincter Reflexes in Patients With Supraesophageal Reflux Disease

Variability in the muscle composition of rat esophagus and neural pathway of lower esophageal sphincter relaxation

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