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Ann Thorac Surg 2005;79:1126-1131
© 2005 The Society of Thoracic Surgeons

Original articles: General thoracic

Effect of Lower Esophageal Sphincter Distension and Acidification on Esophageal Pressure and Electromyographic Activity: The Identification of the "Sphinctero-Esophageal Excitatory Reflex"

Ahmed Shafik, MD, PhDa,*, Ismail Shafik, MD, MCha, Olfat El-Sibai, MD, PhDb, Randa Mostafa, MD, PhDc

a Department of Surgery and Experimental Research, Faculty of Medicine, Cairo University, Cairo, Egypt
b Department of Surgery, Faculty of Medicine, Menoufia University, Shebin El-Kom, Egypt
c Department of Physiology, Faculty of Medicine, Zagazig University, Benha, Egypt

Accepted for publication September 27, 2004.

* Address reprint requests to Dr A. Shafik, 2 Talaat Harb Street, Cairo, 11121, Egypt (E-mail: shafik{at}ahmed-shafik.org).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: The mechanism of esophageal acid clearance through augmenting esophageal peristalsis in response to gastroesophageal reflux (GER) is not exactly known. We investigated the hypothesis that lower esophageal sphincter (LES) dilatation rather than the refluxed acid affected reflex increase in the esophageal peristaltic activity aiming at clearing the esophagus of the refluxed acid.

METHODS: The esophageal pressure and electromyographic (EMG) activity response to esophageal sphincter balloon distension in increments of 2 mL of saline was recorded in 17 healthy volunteers (10 men, 7 women, mean age 43.6 ± 11.2 years). The test was repeated in 10 of 17 volunteers while the esophageal sphincter was being anesthetized. The response of the esophageal pressure and electromyographic activity to lower esophageal acidification was also tested.

RESULTS: Lower esophageal sphincter balloon distension with 2 mL of saline produced esophageal pressure increase to a mean of 34.2 ± 5.3 cm H2O (p < 0.001). Increase of the balloon distending volume produced results similar to the 2-mL distension (p > 0.05). The esophageal electrical activity increased on esophageal balloon distension; the increase was similar with distensions of 2 mL up to 10 mL. There was no esophageal pressure or electrical activity response to distension of the anesthetized lower esophageal sphincter or to lower esophageal sphincter acidification.

CONCLUSIONS: During gastroesophageal reflux episodes, the lower esophageal sphincter dilatation and not acidification appears to initiate increased esophageal peristalsis, which clears the esophagus of the refluxed acid. The increased esophageal peristalsis on lower esophageal sphincter dilatation is suggested to be reflex in nature and is mediated through the "sphincteroesophageal excitatory reflex." This reflex may be of diagnostic significance in esophageal motility disorders; however, this point needs further studies.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
The esophagus transports food and fluid from the pharynx to the stomach. A sphincteric action exists within the lowermost 4 cm of the esophagus, which prevents reflux of gastric contents into the esophagus [1, 2]. The mechanism of gastroesophageal competence is complex and not completely understood [3–6]. A true anatomical sphincter could not be demonstrated at the lower end of the esophagus, and the existing sphincteric action is considered a physiologic one [7–9].

The lower esophagus has a barrier function, meaning that the existing high-pressure zone in the lower esophageal sphincter (LES) has the ability to prevent gastroesophageal reflux (GER) [1–6]. The diaphragm is believed to play a contributory role in this barrier function [3–6]. A normal tendency to GER prevails because the resting pressure in the esophageal body (–5 mm Hg) is lower than the resting pressure in the stomach fundus (+5 mm Hg). This tendency is overcome by the tonic contraction of the LES during rest, creating a high-pressure zone of 10 to 35 mm Hg [7–9].

Studies have reported that the normal response to naturally occurring reflux episodes is to increase the swallowing frequency through augmentation of the peristaltic activity [10, 11]. This action quickly clears the esophagus of refluxed acid, diminishing the overall esophageal exposure to gastric juice and the risk of mucosal injury. The increased peristaltic activity seems also to rapidly transmit the associated increased amounts of saliva. In mild esophagitis, the heartburn that accompanies esophageal exposure to acid results in increased salivation and swallowing that clears the esophagus [12–14]. Meanwhile, in advanced reflux disease and Barrett's esophagus, there is a poor swallowing response to refluxed acid and consequently a prolonged exposure to acid and a greater esophageal injury. This compromised swallowing response to reflux seems to be secondary to destruction of mucosal nociceptors by the metaplasic process [12–14].

In reviewing the previous findings, acid clearance in GER disease (GERD) is performed by increasing salivation and the esophageal peristaltic activity. A description of the mechanism of acid clearance by augmenting esophageal peristalsis in response to GER could not be traced in the literature. We hypothesized that LES dilatation rather than the refluxed acid during GER affected reflex increase in the esophageal peristaltic activity, aiming at clearing the esophagus of the refluxed acid. This hypothesis was investigated in the current study.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Acknowledgments
 References
 
Patients
The study was not designed as a randomized, double-blind, placebo-controlled trial. The patients were volunteers who refused to accept payment. Seventeen healthy people (10 men, 7 women, mean age 43.6 ± 11.2 years [standard deviation], age range 31 to 55 years old) volunteered for this study. They had no gastrointestinal complaint in the past or at the time of enrollment. They gave an informed consent after having been fully informed about the nature of the study, the tests to be done, and their role in the study. The Cairo University Review Board and Ethics Committee approved the study.

The results of physical examination, including neurologic assessment, were normal. Laboratory work results including blood count, renal and hepatic function tests as well as electrocardiography were unremarkable.

Methods
The volunteers fasted overnight. Under no anesthesia or sedation, a balloon-tipped tube was introduced into the stomach. The 1.5-cm diameter polyethylene balloon was tied to the distal end of a 6F polyethylene tube. The tube had a metallic ring at its distal end for fluoroscopic control and was connected to a strain gauge pressure transducer (Statham 230 B, Oxnard, CA). The gastric tube was slowly pulled out of the stomach into the esophagus with the aid of an automatic puller, which had been adjusted to withdraw the tube at a rate of 6 cm/min. The pressure readings during the tube withdrawal were noted. The LES was located in the area where pressure readings began to rise. The balloon was placed in the lower esophagus in the area of maximum pressure.

Manometric Studies
A manometric 6F catheter was introduced into the esophagus to lie in the esophagus proper away from the sphincters. The catheter had two side parts and a metallic clip applied to its distal closed end for fluoroscopic control. It was connected to a pneumohydraulic capillary infusion system (Arndorfer Medical Specialties, Greendale, WI). The pump delivered saline solution continuously through the capillary tube at a rate of 0.6 mL/min. The transducer outputs were registered on a rectilinear recorder (Model RS-400; Gould Inc, Cincinnatti, OH). Occlusion of the recording orifice produced a pressure elevation rate that was greater than 250 cm H2O/s. During pressure measurements, the catheter was rotated so as to record anteroposterior and lateral pressures.

Electromyographic Study
The electrical activity of the esophagus was studied by means of monopolar silver-silver chloride electrodes of 0.8-mm diameter (Smith-Kline Becham, Los Angeles, CA). The electrode was situated 1 cm from the tip of a 6F catheter. The catheter was attached to the esophageal mucosa by suction with a negative pressure, which ranged from 50 to 100 mm Hg and was maintained during the test.

Two electrodes were introduced into the esophagus by means of an endoscope; one electrode was applied to the upper third and the other to the lower third of the esophagus. After recording the electrical activity with the electrodes in these positions, the upper electrode was transferred to the middle third of the esophagus and the test was repeated. Signals from the electrodes were fed into an alternating current amplifier with a frequency response within ± 3 dB from 0.016 Hz to 1 kHz; they were displayed on a recorder at a sensitivity of 1 mV/cm. The indifferent electrode was a metallic disc applied to the abdominal skin. A strain gauge respiration transducer was applied to the thoracic wall.

Before starting the tests, a 20-minute period was allowed for the esophagus to adapt to the applied devices.

The balloon at the LES was then distended with normal saline in increments of 2 mL up to 10 mL and the pressure and electromyographic (EMG) activity of the esophagus proper was recorded. The manometric tube was moved in the esophagus to measure the pressure in the upper, middle, and lower esophagus.

Response of the Esophageal Pressure and Electrical Activity to Acidification of the Lower Esophagus
The effect of acidification of the LES on the esophageal pressure and electrical activity was examined using the Bernstein test [15]. A 6F tube was introduced to lie in the LES and a 0.1 N solution of hydrochloric acid was instilled. The esophageal pressure and EMG activity were then recorded at rest and at LES balloon distension with 2-mL increments of normal saline.

Anesthetization of the Lower Esophageal Sphincter
This test was performed in 10 of 17 of the volunteers studied. They gave consent after being informed of the nature of the test. The LES was anesthetized by endoscopically injecting 5 mL of 2% lidocaine circumferentially at multiple points in the LES. The esophageal pressure and EMG activity were recorded after 20 minutes and 3 hours later when the anesthetic effect had waned. The test was repeated using normal saline instead of lidocaine.

To ensure reproducibility of the results, the previously described tests were repeated at least twice in the individual subject and the mean value was calculated. The results were analyzed statistically using the Student's t test, and the values were given as the mean ± standard deviation. Differences assumed significance at p less than 0.05.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Acknowledgments
 References
 
All the volunteers were evaluated. No adverse side effects were encountered during or after the tests.

Effect of LES Balloon Distension on Esophageal Pressure
The basal pressure of the esophagus ranged from –5 to +5 cm H2O. The response of the esophageal pressure to LES balloon distension with 2, 4, 6, 8, and 10 mL of saline is shown in Table 1. Balloon distension with 2 mL of saline affected a significant increase (p < 0.001) of the esophageal pressure to a mean of 34.2 ± 5.3 cm H2O. Meanwhile, distension with 4, 6, 8, and 10 mL of saline produced an esophageal pressure increase similar to the 2-mL distension with no significant differences (p > 0.05, Table 1). The esophageal pressure increase on LES balloon distension remained for 8 to 10 seconds (mean 9.2 ± 0.9) and then dropped to the basal values although the LES balloon distension was continuous. Repetition of the LES distension produced the same esophageal pressure response, provided a lapse period of 8 to 12 seconds (mean 10.6 ± 1.2) had passed between two successive distensions. We obtained no esophageal response if esophageal distension was performed after a shorter period.


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  		Table 1. Esophageal Pressure of 17 Healthy Volunteers on LES Balloon Distension With Saline in Increments of 2 mL up to 10 mLa
 
The latency, which is the time passing from the onset of balloon distension to the onset of esophageal pressure response, varied from 16 to 22 ms (mean 18.4 ± 2.7). There were no significant differences in esophageal pressure response between men and women, or young and elderly volunteers.

Esophageal Pressure Response to Distension of the Anesthetized LES
In the 10 individuals in whom the LES was anesthetized, the esophageal pressure response to LES balloons distension did not occur. After 3 hours, when the lidocaine effect had waned, the esophageal pressure response was similar to that before anesthetization with no significant difference (p > 0.05). Saline injection of the LES did not affect the esophageal pressure response to LES balloon distension.

Effect of LES Balloon Distension on the Electrical Activity of the Esophagus
Slow waves (SWs) at rest (basal) were recorded from the 2 electrodes of each individual. They were monophasic and negatively deflected (Fig 1). The SWs had the same frequency, amplitude, and conduction velocity from the 2 electrodes of the individual subject (Fig 1). The mean frequency was 5.9 ± 1.4 cycle/min (range 4.8 to 7.3), the amplitude 0.48 ± 0.04 mV (range 0.36 to 0.63), and conduction velocity 4.8 ± 1.1 cm/s (range 3.8 to 6.3). These values were the same whether recorded from the upper, mid, or lower third of the esophagus in the individual subject. Bursts of fast activity spikes or action potentials (APs) were superimposed on or followed the SWs randomly. They took the form of negative deflections (Fig 1).



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  		Fig 1. Electroesophagogram of a healthy volunteer at rest showing slow waves with regular rhythm and random action potentials.

 
Esophageal balloon distension with 2 mL of saline affected an increase in the esophageal electrical activity (Table 2, Fig 2). The frequency, amplitude and conduction velocity of the SWs manifested significant increase (p < 0.05, p < 0.05, p < 0.05, respectively); the APs increased randomly (Fig 2). Esophageal balloon distension with 4, 6, 8, and 10 mL of saline produced an increase in the esophageal electrical activity similar to that of the 2-mL distension with no significant difference (p > 0.05, Fig 3). The increase of the electrical activity continued for 7 to 9 seconds (mean 8.6 ± 0.7) and then declined to the basal values although the esophageal balloon was still distended. Repetition of the test produced the same esophageal response, provided a time of more than a mean of 10.8 ± 2.9 seconds (range 8 to 14) had passed between 2 successive distensions. There was no significant difference in esophageal response to esophageal balloon distension between men and women, or between young and elderly volunteers.


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  		Table 2. Electric Waves of the Esophagus Recorded on Esophageal Distension in Increments of 2 mL of Normal Saline up to 10 mLa
 


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  		Fig 2. Electroesophagogram of a healthy volunteer upon lower esophageal balloon distension with 2 mL of normal saline. It shows increased frequency, amplitude, and conduction velocity of the slow waves. ({uparrow} = distension.)

 


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  		Fig 3. Electroesophagogram of a healthy volunteer upon lower esophageal balloon distension with 8 mL of normal saline. It shows increased frequency, amplitude, and conduction velocity of the slow waves similar to those with 2-mL distension. ({uparrow} = distension.)

 
Esophageal Response of the Electrical Activity to Distension of the Anesthetized LES
Balloon distension of the anesthetized LES in 10 volunteers produced no significant change from the basal electrical activity of the esophagus (Fig 4). With waning of the anesthetic effect after 3 hours, the response of the esophageal electrical activity to esophageal distension was similar to that before anesthetization with no significant difference (p > 0.05). Meanwhile, injection of the lower esophagus with saline instead of lidocaine did not affect the esophageal response to esophageal distension.



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  		Fig 4. Electroesophagogram of a healthy volunteer upon balloon distension of the anesthetized lower esophagus showing no significant change from the basic electrical activity. ({uparrow} = distension.)

 
Results of LES Acidification on Esophageal Pressure and EMG Activity
Esophageal perfusion with HCl did not cause a burning sensation to the subjects. It was not associated with significant changes in esophageal pressure or EMG activity (p > 0.05, p > 0.05, respectively). Meanwhile, LES balloon distension with 2, 4, 6, 8, and 10 mL of saline produced results with esophageal pressure and EMG activity similar to those without HCl instillation.

The results were reproducible with no significant difference when the tests were repeated in the individual subject.


   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Acknowledgments
 References
 
The normal response to naturally occurring reflux episodes is excessive salivation as well as increased frequency of swallowing [10, 11]. This action quickly clears the esophagus of the refluxed acid, diminishing the overall esophageal exposure to gastric juice and the risk of mucosal injury. Two events occur during GER: opening of the LES and acid reflux. Under normal physiologic conditions, these events are associated with excessive salivation and swallowing with increased esophageal peristaltic activity [10, 11].

The current findings apparently denote that the LES dilatation initiates the increased peristaltic activity. This is evident from the increase of esophageal pressure and electrical activity on LES balloon distension. The recording of sequential electrical waves from the upper, middle, and lower esophagus seems to denote that these electrical waves are representative of the peristaltic activity of the esophagus. The esophageal pressure and EMG response to LES dilatation did not depend on the distending volume of the LES; the response remained the same with increasing distending volumes. The increased esophageal pressure and EMG activity on LES dilatation presumably indicate the creation of a secondary esophageal peristaltic activity that appears to sweep acid back into the stomach, thus reducing both its volume and the duration of its contact with the esophageal mucosa. This antireflux action of the esophageal peristalsis seems to act through two mechanisms: the peristalsis pushes the refluxed acid back into the stomach, and the peristalsis brings the excessive salivation down the esophagus to neutralize any remaining acid. Although GER initiates esophageal peristalsis and excessive salivation, we believe that peristalsis plays the essential role in clearing the refluxed acid by pumping the saliva down to the LES. Furthermore, in advanced reflux esophagitis, esophageal clearing is aborted following the associated diminished or absent esophageal peristalsis.

It may be argued that balloon dilatation of the LES is not identical with relaxation of the sphincter. However, LES balloon distension was performed to induce dilatation of the LES. The end result of LES dilatation or relaxation is the opening of the sphincter, which leads to acid reflux.

Sphincteroesophageal Excitatory Reflex
The increase of the esophageal pressure and EMG activity on LES dilatation postulates a reflex relationship between the two actions. This relationship is evidenced by reproducibility and by its absence on anesthetization of the LES, which is a suggested arm of the reflex arc; the second arm is presumably the esophageal musculature. Lidocaine blocks the sensory fibers (C and A {alpha}-fibers) that are responsible for pain and reflex activity [16, 17]. We call this reflex relationship "sphincteroesophageal excitatory reflex." It is assumed that LES distension stimulates the stretch receptors in the LES, thereby evoking the reflex contraction of the esophageal musculature. Stretch receptor stimulation does not seem to be affected by the LES distending volume; increase in the LES distending volume has produced the same esophageal responses. Meanwhile, the esophageal response was not reproducible before a certain lapse period had passed between two successive LES distensions. This period appears to represent the time taken by the esophageal peristalsis to reach the LES from the upper esophagus.

The current study has shown that LES dilatation affected a significant increase in the esophageal pressure and EMG activity, while esophageal acidification did not. It is thus apparent that the esophagus responds to LES dilatation and not to esophageal acidification. It is posulated that LES dilatation evokes the esophageal peristalsis, which brings the saliva down to neutralize the refluxed acid.

Under normal physiologic conditions, the GER occurs when the LES opens and acid refluxes into the esophagus. LES distention during reflux evokes the sphincteroesophageal excitatory reflex with a resulting initiation of the esophageal peristaltic activity, which brings the excessively secreted saliva down to neutralize the acid. It seems that the LES is kept open during the esophageal peristaltic activity effected by the esophagosphincteric inhibitory reflex [18]; the latter reflex acts to open the LES. Thus a sequence of events occurs with the start of GER. Opening of the LES on GER presumably evokes the sphincteroesophageal excitatory reflex that initiates the esophageal peristaltic activity. The latter seems to evoke the esophagosphincter inhibitory reflex that keeps the LES open to wash down the refluxed acids by means of the excessive salivation and peristalsis. Hence, with these reflexes that apparently act under normal physiologic conditions there is no possibility for the refluxed material to remain in the esophagus inducing its injurious effects. A disorder of one or the other of these reflexes would disturb the esophageal clearing mechanism with a resulting reflux esophagitis.

Although the design of the study is not a randomized, double-blind, placebo-controlled trial, the methodologies which include manometric measurements and EMG recordings minimize any bias that may arise.

Diagnostic Role of the Sphincteroesophageal Excitatory Reflex
The esophagus, besides being involved in reflux esophagitis, is the site of various motility disorders. Their diagnosis and the differentiation of one type from the other is as yet difficult despite the advances achieved in the esophageal investigative tools. Prolonged latency of the sphincteroesophageal reflex or a change in the slow waves measurements to abnormal values presumably signify a defect in the reflex pathway, which could represent a muscle or nerve damage from a disease of the spinal cord, spinal nerve roots or peripheral nerves. The measuring of latency and the slow waves measurements could thus be an objective and accurate means to demonstrate the intactness of this pathway. We believe that the inclusion of this reflex as a diagnostic tool in esophageal disorders will prove valuable after further studies have been performed to look into this issue.

Conclusions
During GER episodes, the LES dilatation and not acidification appears to initiate increased esophageal peristalsis which acts to clear the esophagus of the refluxed acid. The increased esophageal peristalsis on LES dilatation is suggested to be reflex in nature and mediated through the "sphincteroesophageal excitatory reflex." This reflex may prove to have diagnostic potential in esophageal motility disorders; however, this requires further study.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
References
 
The authors thank Margot Yehia for her assistance in preparing the manuscript.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Cohen S, Harris LD. Lower esophageal sphincter pressure as an index of lower esophageal sphincter strength Gastroenterology 1970;58:157-162.[Medline]
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  3. Nebel OT, Castell DO. Lower esophageal sphincter pressure changes after food ingestion Gastroenterology 1972;63:778-783.[Medline]
  4. Sturdevant RA. Is gastrin the major regulator of lower esophageal sphincter pressure? Gastroenterology 1974;67:551-553.[Medline]
  5. Cohen S, Lipshultz W. Hormonal regulation of human lower esophageal sphincter competenceInteraction of gastrin and secretin. J Clin Invest 1971;50:449-454.
  6. Postlethwait RW. Physiology. In: Surgery of the esophagus2nd ed. Norwalk, CT: Appleton-Century-Crofts; 1986591.
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  9. Korn O, Csenders A, Burdiles I, Stein HJ. Anatomic dilatation of the cardia and competence of the lower esophageal sphincter: a clinical and experimental study J Gastrointest Surg 2000;4:398-406.[Medline]
  10. Helm JF, Dodds WJ, Hogan WJ. Salivary responses to esophageal acid in normal subjects and patients with reflux esophagitis Gastroenterology 1982;93:1393-1397.
  11. Bremner RM, Hoeft SF, Costantini M, Crookes PF, Bremner CG, DeMeester TR. Pharyngeal swallowing: the major factor in clearance of esophageal reflux episodes Ann Surg 1993;218:364-370.[Medline]
  12. Katzka DA, Castell DO. Successful elimination of reflux symptoms does not insure adequate control of acid reflux in patients with Barrett's esophagus Am J Gastroenterol 1994;89:989-991.[Medline]
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  15. Bernstein LM, Baker LA. A clinical test for esophagitis Gastroenterology 1958;34:760-762.[Medline]
  16. Yokoyama O, Komatso, Kodama K, Yotsuyanagi S, Nakura S, Namiki M. Diagnostic value of intravesical lidocaine for overactive bladder J Urol 2000;164:340-344.[Medline]
  17. Silva C, Ribeiro MI, Cruz F. The effect of intravesical resiniferatoxin in patients with idiopathic detrusor instability suggests that involuntary detrusor contractions are triggered by C-fiber input J Urol 2002;168:575-579.[Medline]
  18. Shafik A. Esophago-sphincter inhibitory reflex: role in the deglutition mechanism and esophageal achalasia J Invest Surg 1996;9:37-43.[Medline]




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