scholarly journals A novel pattern of longitudinal muscle contraction with subthreshold pharyngeal stimulus: a possible mechanism of lower esophageal sphincter relaxation

2012 ◽  
Vol 302 (5) ◽  
pp. G542-G547 ◽  
Author(s):  
Eric Leslie ◽  
Valmik Bhargava ◽  
Ravinder K. Mittal

A subthreshold pharyngeal stimulus induces lower esophageal sphincter (LES) relaxation and inhibits progression of ongoing peristaltic contraction in the esophagus. Recent studies show that longitudinal muscle contraction of the esophagus may play a role in LES relaxation. Our goal was to determine whether a subthreshold pharyngeal stimulus induces contraction of the longitudinal muscle of the esophagus and to determine the nature of this contraction. Studies were conducted in 16 healthy subjects. High resolution manometry (HRM) recorded pressures, and high frequency intraluminal ultrasound (HFIUS) images recorded longitudinal muscle contraction at various locations in the esophagus. Subthreshold pharyngeal stimulation was induced by injection of minute amounts of water in the pharynx. A subthreshold pharyngeal stimulus induced strong contraction and caudal descent of the upper esophageal sphincter (UES) along with relaxation of the LES. HFIUS identified longitudinal muscle contraction of the proximal (3–5 cm below the UES) but not the distal esophagus. Pharyngeal stimulus, following a dry swallow, blocked the progression of dry swallow-induced peristalsis; this was also associated with UES contraction and descent along with the contraction of longitudinal muscle of the proximal esophagus. We identify a unique pattern of longitudinal muscle contraction of the proximal esophagus in response to subthreshold pharyngeal stimulus, which we propose may be responsible for relaxation of the distal esophagus and LES through the stretch sensitive activation of myenteric inhibitory motor neurons.

2018 ◽  
Vol 315 (5) ◽  
pp. G734-G742 ◽  
Author(s):  
Arash Babaei ◽  
Ravinder Mittal

Cholecystokinin (CCK) is known to cause lower esophageal sphincter (LES) relaxation through the activation of inhibitory motor neurons. CCK receptor agonists increase the frequency of transient LES relaxation through a peripheral mechanism. Recent studies show that the longitudinal muscle contraction (LMC)-related axial stretch might play a role in the LES relaxation by activating the mechanosensitive inhibitory motor neurons. The aim of our study was to determine whether the CCK-induced LES relaxation and the characteristics of LMC resemble those seen with spontaneous transient LES relaxation in humans. Nine healthy volunteers (5 Fr, 40 ± 12 yr) received escalating doses of CCK-octapeptide (CCK-8) (5, 10, 20, and 40 ng/kg). All subjects demonstrated a monophasic response to 5 ng/kg of CCK-8. In the majority of subjects, this response consisted of partial LES relaxation. All subjects showed a biphasic response to 40 ng/kg of CCK-8. The latter in most subjects consisted of 1) a period of partial relaxation followed by 2) complete LES relaxation along with crural diaphragm inhibition. The length of the esophagus decreased by 0.9 ± 0.4 cm, and muscle thickness increased by 40 ± 14% to 1.4 ± 0.2 mm ( P < 0.05) during initial partial LES relaxation. During complete LES relaxation there was greater LMC, as demonstrated by an esophageal shortening of 1.9 ± 0.5 cm and an increase in muscle thickness of 100 ± 16% ( P < 0.01). The complete phase 2 LES relaxation typically terminated with a robust after-contraction. Atropine significantly attenuated the CCK-induced esophageal LMC, prevented crural diaphragm inhibition, and abolished the phase 2 complete LES relaxation.NEW & NOTEWORTHY The phenotypic features of CCK-induced longitudinal muscle contraction (LMC), complete lower esophageal sphincter (LES) relaxation, and crural diaphragm inhibition, followed by a robust after-contraction, resemble those seen during spontaneous transient LES relaxation. A strong temporal relationship between the LMC and complete transient LES relaxation supports our hypothesis that the LMC plays an important role in the LES relaxation and crural diaphragmatic inhibition.


2001 ◽  
Vol 120 (5) ◽  
pp. A632
Author(s):  
Guoxiang Shi ◽  
John E. Pandolfino ◽  
Raymond J. Joehl ◽  
James G. Brassuer ◽  
Peter J. Kahrilas

1991 ◽  
Vol 261 (6) ◽  
pp. G974-G980 ◽  
Author(s):  
S. S. Harrington ◽  
W. J. Dodds ◽  
R. K. Mittal

The aim of this study was to characterize lower esophageal sphincter (LES) longitudinal muscle contraction during changes in LES pressure in opossums. LES pressure was used as a marker of LES circular muscle contraction. Longitudinal muscle contraction was measured by strain gauge transducers. For precise placement of the strain gauge on the LES, the high-pressure zone was identified using a manometric-laser illumination technique. Measurements were made during 1) spontaneous LES pressure fluctuations, 2) LES pressure changes induced by pharmacological agents, and 3) LES relaxation induced by vagal nerve stimulation. These studies show that 1) spontaneous LES pressure fluctuations correlated with spontaneous changes in LES longitudinal muscle contraction; 2) pharmacologically induced contraction and relaxation of LES pressure correlated with contraction and relaxation of LES longitudinal muscle, respectively; 3) a close temporal relationship existed between changes in LES longitudinal muscle contraction and LES pressure that occurred spontaneously or were induced pharmacologically; and 4) vagal stimulation caused LES longitudinal muscle contraction and LES pressure relaxation. We propose that LES longitudinal muscle may play a role in the modulation of intraluminal LES pressure.


2008 ◽  
Vol 134 (5) ◽  
pp. 1322-1331 ◽  
Author(s):  
Arash Babaei ◽  
Valmik Bhargava ◽  
Hariprasad Korsapati ◽  
Wei Hao Zheng ◽  
Ravinder K. Mittal

2012 ◽  
Vol 302 (3) ◽  
pp. G389-G396 ◽  
Author(s):  
Monika A. Kwiatek ◽  
Frédéric Nicodème ◽  
John E. Pandolfino ◽  
Peter J. Kahrilas

This study aimed to apply novel high-resolution manometry with eight-sector radial pressure resolution (3D-HRM technology) to resolve the deglutitive pressure morphology at the esophagogastric junction (EGJ) before, during, and after bolus transit. A hybrid HRM assembly, including a 9-cm-long 3D-HRM array, was used to record EGJ pressure morphology in 15 normal subjects. Concurrent videofluoroscopy was used to relate bolus movement to pressure morphology and EGJ anatomy, aided by an endoclip marking the squamocolumnar junction (SCJ). The contractile deceleration point (CDP) marked the time at which luminal clearance slowed to 1.1 cm/s and the location (4 cm proximal to the elevated SCJ) at which peristalsis terminated. The phrenic ampulla spanned from the CDP to the SCJ. The subsequent radial and axial collapse of the ampulla coincided with the reconstitution of the effaced and elongated lower esophageal sphincter (LES). Following ampullary emptying, the stretched LES (maximum length 4.0 cm) progressively collapsed to its baseline length of 1.9 cm ( P < 0.001). The phrenic ampulla is a transient structure comprised of the stretched, effaced, and axially displaced LES that serves as a “yield zone” to facilitate bolus transfer to the stomach. During ampullary emptying, the LES circular muscle contracts, and longitudinal muscle shortens while that of the adjacent esophagus reelongates. The likely LES elongation with the formation of the ampulla and shortening to its native length after ampullary emptying suggest that reduction in the resting tone of the longitudinal muscle within the LES segment is a previously unrecognized component of LES relaxation.


2018 ◽  
Vol 91 (1) ◽  
pp. 120-128
Author(s):  
Marcus Joachim Herzig ◽  
Radu Tutuian

Esophageal achalasia is a primary smooth muscle motility disorder specified by aperistalsis of the tubular esophagus in combination with a poorly relaxing and occasionally hypertensive lower esophageal sphincter (LES). These changes occur secondary to the destruction of the neural network coordinating esophageal peristalsis and LES relaxation (plexus myentericus). There are limited data on segmental involvement of the esophagus in adults.We report on the case of a 54-year-old man who presented initially with complete aperistalsis limited to the distal esophagus. After a primary good response to BoTox-infiltration of the distal esophagus the patient relapsed two years later. The manometric recordings documented now a progression of the disease with a poorly relaxing hypertensive lower esophageal sphincter and complete aperistalsis of the tubular esophagus (type III achalasia according to the Chicago 3.0 classification system).This paper also reviews diagnostic findings (including high resolution manometry, CT scan, barium esophagram, upper endoscopy and upper endoscopic ultrasound data) in patients with achalasia and summarizes the therapeutic options (including pneumatic balloon dilatation, botulinum toxin injection, surgical or endoscopic myotomy).


2005 ◽  
Vol 288 (5) ◽  
pp. G927-G932 ◽  
Author(s):  
Jianmin Liu ◽  
James L. Puckett ◽  
Torahiko Takeda ◽  
Hwoon-Yong Jung ◽  
Ravinder K. Mittal

Esophageal distension causes simultaneous relaxation of the lower esophageal sphincter (LES) and crural diaphragm. The mechanism of crural diaphragm relaxation during esophageal distension is not well understood. We studied the motion of crural and costal diaphragm along with the motion of the distal esophagus during esophageal distension-induced relaxation of the LES and crural diaphragm. Wire electrodes were surgically implanted into the crural and costal diaphragm in five cats. In two additional cats, radiopaque markers were also sutured into the outer wall of the distal esophagus to monitor esophageal shortening. Under light anesthesia, animals were placed on an X-ray fluoroscope to monitor the motion of the diaphragm and the distal esophagus by tracking the radiopaque markers. Crural and costal diaphragm electromyograms (EMGs) were recorded along with the esophageal, LES, and gastric pressures. A 2-cm balloon placed 5 cm above the LES was used for esophageal distension. Effects of baclofen, a GABAB agonist, were also studied. Esophageal distension induced LES relaxation and selective inhibition of the crural diaphragm EMG. The crural diaphragm moved in a craniocaudal direction with expiration and inspiration, respectively. Esophageal distension-induced inhibition of the crural EMG was associated with sustained cranial motion of the crural diaphragm and esophagus. Baclofen blocked distension-induced LES relaxation and crural diaphragm EMG inhibition along with the cranial motion of the crural diaphragm and the distal esophagus. There is a close temporal correlation between esophageal distension-mediated LES relaxation and crural diaphragm inhibition with the sustained cranial motion of the crural diaphragm. Stretch caused by the longitudinal muscle contraction of the esophagus during distension of the esophagus may be important in causing LES relaxation and crural diaphragm inhibition.


2010 ◽  
Vol 298 (5) ◽  
pp. G601-G607 ◽  
Author(s):  
Arash Babaei ◽  
Valmik Bhargava ◽  
Ravinder K. Mittal

Although some studies show that the upper esophageal sphincter (UES) contracts during transient lower esophageal sphincter relaxation (TLESR), others show that it relaxes. We hypothesized that the posture of the subject and constituents of gastroesophageal reflux (GER) may determine the type of UES response during the TLESR. High-resolution manometry and esophageal pH/impedance recording were performed in 10 healthy volunteers in the right recumbent (1 h) and upright (1 h) positions following the ingestion of a 1,000-Kcal meal. The UES pressure response during TLESR and constituents of GER (liquid, air, and pH) were determined. 109 TLESRs (58 upright and 51 recumbent) were analyzed. The majority of TLESRs were associated with GER (91% upright and 88% recumbent) events. UES relaxation was the predominant response during upright position (81% of TLESRs), and it was characteristically associated with presence of air in the reflux (92%). On the other hand, UES contraction was the predominant response during recumbent position (82% of TLESRs), and it was mainly associated with liquid reflux (71%). The rate of esophageal pressure increase (dP/d t) during the GER, but not the pH, had major influence on the type of UES response during TLESR. The dP/d t during air reflux (127 ± 39 mmHg/s) was significantly higher than liquid reflux (31 ± 6 mmHg/s, P < 0.0001). We concluded that the nature of UES response during TLESR, relaxation or contraction, is related to the posture and the constituents of GER. We propose that the rapid rate of esophageal pressure increase associated with air reflux determines the UES relaxation response to GER.


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