Esophageal wall blood perfusion during contraction and transient lower esophageal sphincter relaxation in humans

We recently reported that esophageal contraction reduces esophageal wall perfusion in an animal study. Our aim was to determine esophageal wall blood perfusion (EWBP) during esophageal contraction and transient lower esophageal sphincter relaxations (TLESRs) in humans. We studied 12 healthy volunteers. A custom-designed laser Doppler probe was anchored to the esophageal wall, 4–6 cm above the LES, by use of the Bravo pH system so that the laser light beam stay directed toward the esophageal mucosa. A high-resolution manometry equipped with impedance electrodes recorded esophageal pressures and reflux events. Synchronized pressure, impedance, pH, and EWBP recordings were obtained during dry and wet swallows and following a meal. Stable recordings of laser Doppler EWBP were only recorded when the laser Doppler probe was firmly anchored to the esophageal wall. Esophageal contractions induced by dry and wet swallows resulted in 46 ± 9% and 60 ± 10% reduction in the EWBP, respectively (compared to baseline). Reduction in EWBP was directly related to the amplitude (curvilinear fit) and duration of esophageal contraction. Atropine reduced the esophageal contraction amplitude and decreased the EWBP reduction associated with esophageal contraction. TLESRs were also associated with reduction in the EWBP, albeit of smaller amplitude (29 ± 3%) but longer duration (19 ± 2 s) compared with swallow-induced esophageal contractions. We report 1) an innovative technique to record EWBP for extended time periods in humans and 2) contraction of circular and longitudinal muscle during peristalsis and selective longitudinal muscle contraction during TLESR causes reduction in the EWBP; 3) using our innovative technique, future studies may determine whether esophageal wall ischemia is the cause of esophageal pain/heartburn.

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Effect of esophageal contraction on esophageal wall blood perfusion

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00293.2011 ◽

2011 ◽

Vol 301 (6) ◽

pp. G1093-G1098 ◽

Cited By ~ 15

Author(s):

Ravinder K. Mittal ◽

Valmik Bhargava ◽

Harshal Lal ◽

Yanfen Jiang

Keyword(s):

Electrical Stimulation ◽

Blood Perfusion ◽

Laser Doppler ◽

Esophageal Wall ◽

Esophageal Mucosa ◽

Experimental Conditions ◽

Doppler Probe ◽

Perfusion Studies ◽

Esophageal Contraction ◽

Stimulation Of

Myocardial blood flow occurs during the diastolic phase of the cardiac cycle, because myocardial contraction during the systolic phase impedes myocardial perfusion. Using laser Doppler perfusion technique, we studied the effect of esophageal contraction on the esophageal wall perfusion. Studies were conducted in rats. A laser Doppler probe was anchored to the esophageal wall, and wall perfusion was studied under various experimental conditions. Increase and decrease in the systemic blood pressure induced by different pharmacological agents was associated with the increase and decrease in the esophageal wall perfusion, respectively. Esophageal contractions induced by electrical stimulation of the vagus nerve and electrical stimulation of the muscle directly resulted in a reduction in the esophageal wall perfusion, in a dose-dependent fashion. Esophageal wall perfusion could be monitored by placing the Doppler probe on the esophageal mucosa or on the outside of the esophageal wall. Esophageal contraction impedes entry of blood into the esophageal wall. Future studies may investigate if ischemia of the esophageal wall induced by sustained esophageal contractions/esophageal spasm is the cause of esophageal pain symptoms in humans.

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479 Esophageal Contraction & Transient Lower Esophageal Sphincter Relaxations are Associated With Reduction in Esophageal Wall Blood Perfusion in Humans

Gastroenterology ◽

10.1016/s0016-5085(12)60384-9 ◽

2012 ◽

Vol 142 (5) ◽

pp. S-101-S-102

Author(s):

Yanfen Jiang ◽

Young Sun Kim ◽

Valmik Bhargava ◽

Ravinder K. Mittalr

Keyword(s):

Lower Esophageal Sphincter ◽

Blood Perfusion ◽

Esophageal Wall ◽

Esophageal Sphincter ◽

Esophageal Contraction

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Circular and longitudinal muscles shortening indicates sliding patterns during peristalsis and transient lower esophageal sphincter relaxation

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00067.2015 ◽

2015 ◽

Vol 309 (5) ◽

pp. G360-G367 ◽

Cited By ~ 5

Author(s):

Nirali Patel ◽

Yanfen Jiang ◽

Ravinder K. Mittal ◽

Tae Ho Kim ◽

Melissa Ledgerwood ◽

...

Keyword(s):

Lower Esophageal Sphincter ◽

Animal Studies ◽

Longitudinal Muscle ◽

Circular Muscle ◽

Esophageal Sphincter ◽

And Function ◽

Longitudinal Muscles ◽

Histology And Immunohistochemistry ◽

Esophageal Contraction ◽

Axial Shortening

Esophageal axial shortening is caused by longitudinal muscle (LM) contraction, but circular muscle (CM) may also contribute to axial shortening because of its spiral morphology. The goal of our study was to show patterns of contraction of CM and LM layers during peristalsis and transient lower esophageal sphincter (LES) relaxation (TLESR). In rats, esophageal and LES morphology was assessed by histology and immunohistochemistry, and function with the use of piezo-electric crystals and manometry. Electrical stimulation of the vagus nerve was used to induce esophageal contractions. In 18 healthy subjects, manometry and high frequency intraluminal ultrasound imaging during swallow-induced esophageal contractions and TLESR were evaluated. CM and LM thicknesses were measured (40 swallows and 30 TLESRs) as markers of axial shortening, before and at peak contraction, as well as during TLESRs. Animal studies revealed muscular connections between the LM and CM layers of the LES but not in the esophagus. During vagal stimulated esophageal contraction there was relative movement between the LM and CM. Human studies show that LM-to-CM (LM/CM) thickness ratio at baseline was 1. At the peak of swallow-induced contraction LM/CM ratio decreased significantly (<1), whereas the reverse was the case during TLESR (>2). The pattern of contraction of CM and LM suggests sliding of the two muscles. Furthermore, the sliding patterns are in the opposite direction during peristalsis and TLESR.

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Axial stretch: a novel mechanism of the lower esophageal sphincter relaxation

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00351.2006 ◽

2007 ◽

Vol 292 (1) ◽

pp. G329-G334 ◽

Cited By ~ 33

Author(s):

Ibrahim Dogan ◽

Valmik Bhargava ◽

Jianmin Liu ◽

Ravinder K. Mittal

Keyword(s):

Muscle Contraction ◽

Lower Esophageal Sphincter ◽

Longitudinal Muscle ◽

Mechanical Stretch ◽

Esophageal Wall ◽

Axial Stretch ◽

Silicon Tube ◽

Nitric Oxide Inhibitor ◽

Esophageal Sphincter

Swallow and esophageal distension-induced relaxations of the lower esophageal sphincter (LES) are associated with an orad movement of the LES because of a concurrent esophageal longitudinal muscle contraction. We hypothesized that the esophageal longitudinal muscle contraction induces a cranially directed mechanical stretch on the LES and therefore studied the effects of a mechanical stretch on the LES pressure. In adult opossums, a silicon tube was placed via mouth into the esophagus and laparotomy was performed. Two needles with silk sutures were passed, 90° apart, through the esophageal walls and silicon tube, 2 cm above the LES. The tube was withdrawn, and one end of each of the four sutures was anchored to the esophageal wall and the other end exited through the mouth to exert graded cranially directed stretch on the LES by using pulley and weights. A cranially directed stretch caused LES relaxation, and with the cessation of stretch there was recovery of the LES pressure. The degree an d duration of LES relaxation increased with the weight and the duration of stretch, respectively. The mean LES relaxation in all animals was 77.7 ± 4.7%. The required weight to induce maximal LES relaxation differed in animals (714 ± 348 g). NG-nitro-L-arginine, a nitric oxide inhibitor, blocked the axial stretch-induced LES relaxation almost completely (from 78 to 19%). Our data support the presence of an axial stretch-activated inhibitory mechanism in the LES. The role of axial stretch in the LES relaxation induced by swallow and esophageal distension requires further investigation.

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Esophageal longitudinal muscle contraction: Another component of transient lower esophageal sphincter relaxation (tLESR)?

Gastroenterology ◽

10.1016/s0016-5085(08)83141-1 ◽

2001 ◽

Vol 120 (5) ◽

pp. A632

Author(s):

Guoxiang Shi ◽

John E. Pandolfino ◽

Raymond J. Joehl ◽

James G. Brassuer ◽

Peter J. Kahrilas

Keyword(s):

Muscle Contraction ◽

Lower Esophageal Sphincter ◽

Longitudinal Muscle ◽

Lower Esophageal Sphincter Relaxation ◽

Esophageal Sphincter

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Identification of longitudinal muscle activity in opossum lower esophageal sphincter

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1991.261.6.g974 ◽

1991 ◽

Vol 261 (6) ◽

pp. G974-G980 ◽

Cited By ~ 1

Author(s):

S. S. Harrington ◽

W. J. Dodds ◽

R. K. Mittal

Keyword(s):

Muscle Contraction ◽

Lower Esophageal Sphincter ◽

Strain Gauge ◽

Longitudinal Muscle ◽

Pressure Fluctuations ◽

Circular Muscle ◽

Pharmacological Agents ◽

Esophageal Sphincter ◽

High Pressure Zone ◽

Contraction And Relaxation

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.

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Mechanism of UES relaxation initiated by gastric air distension

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00120.2014 ◽

2014 ◽

Vol 307 (4) ◽

pp. G452-G458 ◽

Cited By ~ 7

Author(s):

Ivan M. Lang ◽

Bidyut K. Medda ◽

Reza Shaker

Keyword(s):

Time Delay ◽

Lower Esophageal Sphincter ◽

Gastroesophageal Junction ◽

Esophageal Pressure ◽

Upper Esophageal Sphincter ◽

Gastric Fistula ◽

Esophageal Mucosa ◽

Rapid Injection ◽

Free Air ◽

Esophageal Sphincter

The aim of this study was to determine the mechanism of initiation of transient upper esophageal sphincter relaxation (TUESR) caused by gastric air distension. Cats ( n = 31) were decerebrated, EMG electrodes were placed on the cricopharyngeus, a gastric fistula was formed, and a strain gauge was sewn on the lower esophageal sphincter ( n = 8). Injection of air (114 ± 13 ml) in the stomach caused TUESR ( n = 18) and transient lower esophageal sphincter relaxation (TLESR, n = 6), and this effect was not significantly ( P > 0.05) affected by thoracotomy. Free air or bagged air ( n = 6) activated TLESR, but only free air activated TUESR. Closure of the gastroesophageal junction blocked TUESR (9/9), but not TLESR (4/4), caused by air inflation of the stomach. Venting air from distal esophagus during air inflation of the stomach prevented TUESR ( n = 12) but did not prevent air escape from the stomach to the esophagus ( n = 4). Rapid injection of air on the esophageal mucosa always caused TUESR (9/9) but did not always (7/9) cause an increase in esophageal pressure. The time delay between the TUESR and the rapid air pulse was significantly more variable ( P < 0.05) than the time delay between the rapid air pulse and the rise in esophageal pressure. We concluded that the TUESR caused by gastric air distension is dependent on air escape from the stomach, which stimulates receptors in the esophagus, but is not dependent on distension of the stomach or esophagus, or the TLESR. Therefore, the TUESR caused by gastric air distension is initiated by stimulation of receptors in the esophageal mucosa.

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Oxygen uptake and mechanical tension in esophageal smooth muscle from opossums and cats

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1982.242.3.g258 ◽

1982 ◽

Vol 242 (3) ◽

pp. G258-G262

Author(s):

K. Schulze-Delrieu ◽

S. A. Crane

Keyword(s):

Smooth Muscle ◽

Lower Esophageal Sphincter ◽

Longitudinal Muscle ◽

Muscle Tension ◽

Base Line ◽

O2 Consumption ◽

Temperature Dependent ◽

Mechanical Tension ◽

Esophageal Sphincter ◽

Esophageal Muscle

In 44 opossums and 4 cats weighing 1.5-2.5 kg, measurements of O2 consumption were made on esophageal muscle strips using a modified Clark-type polarograph. All strips were cut in the transverse axis of the esophagus and comprised the circular and longitudinal muscle layers and intrinsic nerves. Strips were 20 mm long, 2 mm wide, and less than 0.5 mm thick. The average uptake by all strips was less than 5 microliters O2 . mg dry muscle-1.h-1 at 37 degrees C and was temperature dependent (Q10, 2.2). There was no difference in base-line O2 consumption between strips coming from the proximal, middle, or distal third of the esophageal body and strips coming from the lower esophageal sphincter. Increases in length or tension increased the O2 consumption by sphincter strips but had no effect on body strips. Carbachol (10(-5) M) led to increases of base-line muscle tension and O2 consumption in both sphincter and body strips. Isoproterenol (10(-6) M) decreased the baseline tension and O2 consumption in sphincter strips only. The maintenance of a high basal tension by the lower esophageal sphincter is oxygen dependent and therefore an active muscular process. Also, no gradient of metabolic activity can be demonstrated along the smooth muscle segment of the esophagus.

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