Hypertensive lower esophageal sphincter

This editorial comments on the significance of studies accomplished by Dr. Nahum Freidin, et al, concerning the hypertensive lower esophageal sphincter, and published in the July issue ofDigestive Diseases and Sciences (Freidin N, Traube M, Mittal R, McCallum R: The hypertensive lower esophageal sphincter. Manometric and clinical aspects. Dig Dis Sci 34:1063–1067, 1989).     

Correlation of lower esophageal mucosal ring and lower esophageal sphincter pressure

We assessed the relationship of lower esophageal sphincter pressure (LESP) to presence and absence of lower esophageal mucosal ring (LEMR) in 66 patients to determine if the LEMR was more likely related to prolonged sphincter hypotension. This potential relationship is of interest because LEMR may be due to reflux esophagitis. Each patient had radiographic and manometric studies, and both examinations were done within one week of each other. The mean LESP in patients with LEMR was 23.8 mm Hg (range 4.2–64 mm Hg) compared to 28.7 mm Hg (range 8–59 mm Hg) in patients without LEMR; the difference was not statistically significant. Patients with LEMR were also divided into three subgroups according to the diameter of the rings (13 mm, 14–19 mm, 20 mm). There was no significant relationship between the caliber of LEMR and LESP (P>0.05). Presence of LEMR did not affect the amplitude or duration of primary esophageal peristalsis. These results do not support a relationship between LEMR and prolonged LESP hypotension or abnormal esophageal motility. However, other pathogenetic mechanisms involved in producing reflux esophagitis not related to prolonged sphincter hypotension were not studied.     

The hypertensive lower esophageal sphincter

Controversy exists as to whether the hypertensive lower esophageal sphincter (HLES) represents a clinical motility disorder of the esophagus or is merely the right-sided expression of a normal distribution curve. In the present study we describe 16 patients with HLES, defined as a lower esophageal sphincter (LES) pressure of 40 mm Hg (mean +3sd of controls) with normal peristalsis. All of the patients suffered from chest pain and nine from dysphagia. Delayed bolus transit at the gastroesophageal junction was demonstrated in four patients by radiography. Manometric studies showed that during swallowing the LES residual pressures were significantly greater (9.2±5.0 mm Hg) than observed in normal controls (1.8±2.2 mmHg) (mean±1sd). However, the percent LES relaxation in patients did not differ significantly from controls. Clinical improvement was associated with pharmacological or mechanical reduction of resting LES pressure with an accompanying fall in the nadir pressure. These observations suggest that HLES may have clinical and pathophysiological significance and that evidence for the entity should be sought during manometric studies in the clinical laboratory.     

Stimulation of the incompetent lower esophageal sphincter

The primary function of the lower esophageal sphincter (LES) is to prevent the reflux of gastric contents into the esophagus. We have studied the effect of hormonal and pharmacologic stimuli on LES pressure in patients with symptomatic gastroesophageal reflux due to LES incompetence. Gastric alkalinization, subcutaneous pentagastrin, intravenous edrophonium, and subcutaneous bethanecol each resulted in marked increases in LES pressure. In all studies, pressure rose to a level occurring in normal subjects. Subsequently, the patients were given 25 mg bethanecol orally and pressure monitored for 2 hours. The LES pressure increased from a mean basal pressure of 5.6±0.8 mmHg to a peak of 16.9±2.8 mmHg at 50 minutes. Pressure remained elevated for the full 2-hour study period. Both subcutaneous and oral bethanecol successfully increased LES pressure in all patients with symptomatic reflux to the level of resting pressure seen in normal subjects. These studies suggest a potential role for cholinergic agents in the therapy of symptomatic gastroesophageal reflux.The opinions expressed herein are those of the authors and cannot be construed as reflecting the views of the Navy Department or of the Naval Service at large.Presented at the 53 rd Annual Session of the American College of Physicians, April 19, 1972, Atlantic City, New Jersey.     

Resting pressures in the lower esophageal sphincter

Interdeglutive pressures of the lower esophageal sphincter (LES) were studied by nonpullthrough techniques in 36 volunteers. Resting pressures did not remain at the high levels observed when the LES was entered. In 30 studies a gradual protracted decay ranging from 5 to 18 mm Hg was observed. These studies suggest that the LES may not pose a continuous barrier to reflux of gastric contents.     

Transient lower esophageal sphincter relaxation and the related esophageal motor activities

Transient lower esophageal sphincter (LES) relaxation (TLESR) is defined as LES relaxation without a swallow. TLESRs are observed in both of the normal individuals and the patients with gastroesophageal reflux disorder (GERD). However, TLESR is widely considered as the major mechanism of the GERD. The new equipments such as high resolution manometry and impedance pH study is helped to understand of TLESR and the related esophageal motor activities. The strong longitudinal muscle contraction was observed during development of TLESR. Most of TLESRs are terminated by TLESR related motor events such as primary peristalsis and secondary contractions. The majority of TLESRs are associated with gastroesophageal reflux. Upper esophageal sphincter (UES) contraction is mainly associated with liquid reflux during recumbent position and UES relaxation predominantly related with air reflux during upright position. The frequency of TLESR in GERD patients seems to be not different compared to normal individuals, but the refluxate of GERD patients tend to be more acidic during TLESR.     

Muscular equivalent of the lower esophageal sphincter.

In order to measure muscle thickness and to define the muscular architecture at the gastroesophageal function, both en bloc fixation and a new method of preparing dried fiber specimens were used. Specimens were obtained from 32 kidney donors and human cadavers. Wall thickness was measured at 32 identical locations in the esophagus and stomach. The oblique gastroesophageal ring (GER) was the site of greatest muscular thickness and served as a reference point. From the GER the muscle thickness tapered (P less than 0.05 to P less than 0.001) in both a cephalic (esophageal) and caudal (gastric) direction for a length of 31 mm +/- 2.5 SD. The increase in thickness was due to an increase in the muscle mass (fiber aggregation) of the inner muscle coat. The muscle bundles of this coat split up 10.2 mm +/- 3.0 SD above the GER (fixed specimen) and for a length of 25 mm +/- 8 SD formed short transverse muscle clasps on the lesser curve side. Those muscle bundles on the greater curve side formed long oblique gastric fiber loops. The angle of His was inconstant in location and distal to the uppermost gastric oblique fibers (18 mm +/- 7 SD) and to the GER (9 mm +/- 6 SD).     

Measurement of pressure in the lower esophageal sphincter

Ten healthy human lower esophageal sphincters (LES) were studied with two separate perfused catheter systems, identical in all respects save their external diameters (3.2 and 7 mm for small and large assemblies respectively). Maximum resting pressures, whether recorded by station withdrawal or by slow continous pull-through, were significantly higher with the larger assembly. Residual pressures during postdeglutitive relaxation were similar with the two systems. These observations serve to emphasize that LES pressures recorded with perfused catheters are in fact measurements of the resistance to stretch of sphincteric smooth muscle.     

一过性下食管括约肌松弛与胃食管反流

多年来传统的观念认为下食管括约肌 (ＬＥＳ)屏障功能降低是导致胃食管反流的主要原因。近年来随着上胃肠压力检测技术的发展 ,在卧位状态下对健康志愿者和胃食管反流病 (ＧＥＲＤ)患者进行食管压力和食管 ｐＨ同步监测 ,发现胃食管反流并非均发生于ＬＥＳ压力减低时 ,而常发生在一过性下食管括约肌松弛 (ＴＬＥＳＲ) [1] 。这一发现使得人们对ＧＥＲＤ的病理生理基础进行重新定位 ,同时也能解释为什么有的患者虽然ＬＥＳ压力正常却常常出现反流 ,并为ＧＥＲＤ的治疗提出了新的挑战。虽然对ＴＬＥＳＲ已有多年的研究 ,对ＴＬＥＳＲ有了一定…     

Effects of transdermal nicotine on lower esophageal sphincter and esophageal motility

Cigarette smoking has been shown to decrease lower esophageal sphincter pressure (LESP) by 19–42%. This decrease in LESP may be due to nicotine in the cigarette smoke or substances other than nicotine. The aim of this study was to evaluate the effects of a nicotine patch on esophageal motility since nicotine patches are devoid of all toxins present in the cigarette smoke except the nicotine. Ten healthy nonsmoking volunteers underwent baseline esophageal manometry. Esophageal manometry was repeated after placing a nicotine transdermal patch (Nicotrol) designed to deliver 15 mg of nicotine per day. The parameters that were compared included LESP by rapid pull-through (LESP-RPT) and station pull-through (LESP-SPT), LES relaxation, and velocity, amplitude, and duration of esophageal contractions. Plasma nicotine and cotinine levels were measured prior to baseline manometry and after 12 hr of placing the nicotine patch. the LESP-RPT decreased by 31% from 17.4±6.1 to 12.1±3.3 (P=0.013) and the LESP-SPT by 27% from 13.4±5.4 to 9.8±4.8 (P=0.029) after the nicotine patch. LES relaxation was present in 100% before and after nicotine patch. There were no significant differences in velocity, duration, and amplitude of esophageal contractions after the nicotine patch. Plasma nicotine and cotinine was absent in all subjects at baseline but was significantly elevated after 12 hr of nicotine patch. Transdermal delivery of nicotine results in a significant reduction in LESP in healthy subjects without effecting LES relaxation or esophageal body motility.The opinions and assertions contained herein are the private views of the authors and are not to be construed as reflecting the views of the Department of the Army or the Department of Defense.This work was published in an abstract form in Gastroenterology 106:A1047, 1994.