A test of gastroesophageal sphincter competence

Gastroesophageal manometrics, using continuously perfused polyvinyl tubes, and acid reflux (pH test) were studied prospectively in 13 patients with, and 14, without symptoms and/or signs of gastroesophageal reflux. Pressures were recorded simultaneously from stomach, gastroesophageal sphincter and distal esophagus at rest and during gradual abdominal compression to 80 mm Hg. Neither the mean resting pressures nor the mean increase in gastric or sphincter pressures, during abdominal compression, were significantly different (P>0.10). Sphincteric yield pressures did not separate the 2 groups. However, the mean esophageal pressure rise was significantly greater (P<0.001) in the symptomatic patients (34±4.5 vs 9.9±3.2 mm Hg). The mean pressure in the stomach, sphincter and esophagus became almost identical in the symptomatic patients—a common cavity occurred between stomach and esophagus. Two symptomatic patients had negative pH but positive common cavity tests. No asymptomatic patient had evidence of either reflux or a positive common cavity test.Supported by the Denver Veterans Administration Hospital Training Grant in Gastroenterology, TR 110, and by the National Institute of Health Training Grant in Gastroenterology, AM 5122.     

Lower esophageal sphincter reacts against intraabdominal pressure in children with symptoms of gastroesophageal reflux

Studies of the effect of increased intraabdominal pressure on the lower esophageal sphincter (LES) are controversial. This study aimed to verify the LES competence against extrinsic abdominal compression in children with and without symptoms of gastroesophageal reflux (GER). Eighteen children ages 6–20 months were evaluated, 11 of them with symptoms of GER (group I) and 7 without symptoms of GER (group II). Manometry of the esophagus, LES, and stomach was performed in all children who underwent extrinsic abdominal compressions of 20, 40, 60, and 80 mm Hg. The pressure gradients in the esophagus, LES, and stomach were measured. The pressure gradient showed a significant difference only in the esophagus after extrinsic abdominal compressions of 60 mm Hg [group I median (range): 7.6mm Hg (2.7–20.0) vs group II: 2.8 mm Hg (1.4–9.6), P < 0.05], and 80 mm Hg [group I median (range): 7.7 mm Hg (3.7–28.9) vs group II: 3.8 mm Hg (1.2–21.1), P < 0.05]. It was concluded that the competence of LES to contain increased intraabdominal pressure might be an important factor in the pathophysiology of GER in children.     

Experimental gastroesophageal reflux in the Australian brush-tailed possum.

It has been suggested that the lower esophageal sphincter (LES) plays an important role in preventing gastroesophageal reflux. This study was designed to determine if abolition of the LES alone is sufficient to induce gastroesophageal reflux and esophagitis. Studies were performed in the Australian brush-tailed possum (Trichosurus vulpecula) which has a lower esophagus resembling that of man. Esophageal manometry, esophagoscopy, and contrast radiography of the lower esophagus and stomach were performed before and after surgery in a group of animals undergoing cardioplasty and in a group of sham operated control animals. In the animals undergoing cardioplasty, LES pressure fell from a preoperative level of 12.6 +/- 1.3 mm Hg to 0 mm Hg. This was followed by the development of gastroesophageal reflux and esophagitis. Sham operation did not alter LES pressure or result in either gastroesophageal reflux or esophagitis. In 4 of 5 animals undergoing cardioplasty, LES activity returned after 10 weeks, and this time gastroesophageal reflux ceased and esophagitis healed. It is concluded that abolition of the LES alone can induce gastroesophageal reflux and esophagitis.     

Clinical and manometric findings in benign peptic strictures of the esophagus

To determine the possible factors that may contribute to the development of peptic stricture of the esophagus, clinical and manometric features were compared in patients with symptomatic gastroesophageal reflux and those with peptic strictures of the esophagus. Patients with stricture were older and had a longer duration of heartburn than patients without a stricture. Most importantly, patients with stricture had a more marked decrease in lower esophageal sphincter (LES) pressure, 4.9±0.5 mm Hg, than patients without a stricture, 7.5±0.6 mm Hg, P<0.01. The LES pressure in all patients with stricture was below 8 mm Hg, and did not overlap with normal values. Patients with stricture had either a nonspecific motor abnormality or aperistalsis (64%), compared to patients with symptomatic reflux (32%), P<0.05. Thus, peptic stricture of the esophagus is commonly associated with a long duration of reflux symptoms in patients with a very low LES pressure and esophageal motor disorder.     

Response of canine ileocolonic sphincter to intraluminal acetic acid and colonic distension

The aim was to determine the effect of intraluminal acetic acid and proximal colonic distension on canine ileocolonic sphincter pressure, ileal motility, and coloileal reflux. In six conscious dogs with an isolated ileocolonic loop, basal pressure of the ileocolonic sphincter was similar during ileal perfusion with 100 mM acetic acid at 1 ml/min (mean±sem=18±0.4 mm Hg) and with saline (18±0.5 mm Hg;P=0.81). Discrete clustered ileal contractions were more frequent with acetic acid, however, and when they propagated across the sphincter, sphincter pressure increased from 18±0.4 mm Hg to 36±1.3 mm Hg (P=0.002). Sphincter pressure was also greater during colonic perfusion with acetic acid (32±0.7 mm Hg) than during ileal perfusion with acetic acid or saline (P<0.017). Moreover, sphincter pressure gradually increased as the colon was distended with saline (slope=0.8 mm Hg/cm H₂O,P<0.017) or acetic acid (slope=0.5 mm Hg/cm H₂O,P<0.017), but the increase did not prevent coloileal reflux. In conclusion, ileal clustered contractions, colonic perfusion of acetic acid, and colonic distension all increased canine ileocolonic sphincter pressure.     

The adverse effect of chocolate on lower esophageal sphincter pressure

Decreased lower esophageal sphincter (LES) pressure after ingestion of chocolate has been previously noted. We have further evaluated the effect of chocolate on the known ability of gastric alkalinization or bethanechol to increase LES tone. 9 normal subjects were studied using an infused open-tip recording system. Pressure was monitored for a 15-min basal period, and for 60 min after ingestion of 120 ml of chocolate syrup either alone or with the concurrent administration of commercial antacid, oral bethanechol, or subcutaneous bethanechol. After chocolate ingestion, mean basal LES pressure of 14.6±1.1 (±SEM) mm Hg decreased significantly (P<0.01) to 7.9±1.3 mm Hg. An identical LES response occurred when antacid was given with the chocolate dose. Oral bethanechol (25 mg) and chocolate together resulted in lesser decreases in LES pressure. Subcutaneous bethanechol (5 mg) and chocolate produced significant increases (P<0.05) in sphincter pressure, although of lesser magnitude than reported with bethanechol alone. These results indicate that the adverse effect of chocolate on the LES is not reversed by gastric alkalinization and suggest that bethanechol in sufficient dose may overcome chocolate-induced decreases in LES pressure.This work was supported by the Department of the Navy Clinical Investigation Program Grant #5-05-530R.     

High vasoactive intestinal polypeptide plasma levels in patients with Barrett's esophagus

We have evaluated the correlation between vasoactive intestinal polypeptide (VIP) plasma concentration and severity of gastroesophageal reflux in patients with Barrett's esophagus and the possible differences in the VIP values of these patients compared with healthy volunteers. We also evaluated the relation between VIP plasma concentration and lower esophageal sphincter (LES) pressure in 24 patients with Barrett's esophagus. The mean VIP plasma concentration in 14 patients with severe gastroesophageal reflux was 25.6 +/- 0.75 pg/ml, significantly higher than the mean value observed in 10 patients with moderate reflux (18.9 +/- 0.67 pg/ml) (p less than 0.01). The mean LES resting pressure was significantly lower in the group of patients with severe gastroesophageal reflux than that observed in patients with moderate reflux (3 +/- 0.64 and 10.3 +/- 0.69 mm Hg, respectively; p less than 0.01). The mean VIP plasma concentration in 11 healthy volunteers (20.6 +/- 0.65 pg/ml) was significantly lower than the mean value observed in the subgroup of patients with severe gastroesophageal reflux (p less than 0.01). VIP values in patients with moderate reflux were not significantly different from those observed in our volunteers. There was a significant correlation between LES pressure and VIP plasma level (r = -0.9253; p less than 0.01). In conclusion, it is possible that the decreased LES resting pressure observed in patients with Barrett's esophagus and severe gastroesophageal reflux may be due to impairment of the VIPergic innervation, resulting in an increased local VIP release with possible overflow to peripheral plasma.     

Lower esophageal sphincter pressure in Chagas' disease

It is known that lower esophageal sphincter (LES) pressure in patients with idiopathic achalasia is higher than in normal subjects, but in patients with Chagas' disease, who have esophageal disease with similar clinical, manometric, and radiologic results, studies of LES pressure show contradictory findings. We measured the LES pressure in 118 patients with chronic Chagas' disease, 14 patients with idiopathic achalasia, and 50 control subjects using a perfused catheter and the stationary pull-through (SPT) technique. The patients with Chagas' disease had normal esophageal radiologic examination (group A, N=50), delay in esophageal clearance without dilatation (group B, N=41), or delay in esophageal clearance with dilatation (group C, N=27). The LES pressure of Chagas' disease patients of group A (18.6 ±9.1 mm Hg, mean ±SD), group B (17.8 ±9.7mm Hg), and group C (21.6 ±10.1 mm Hg) was lower (P<0.001) than the LES pressure of the controls (24.9 ±10.2 mm Hg). In patients with idiopathic achalasia, the LES pressure (40.7 ±17.8 mm Hg) was higher than in control subjects (P<0.01) and Chagas' disease patients (P<0.001). We conclude that the LES pressure of patients with Chagas' disease tended to be lower than that of control subjects and achalasia patients.Presented in part at the 8th World Congress of Gastroenterology, September 1986, São Paulo, Brazil, and published in abstract form inDig Dis Sci 31:273, 1986.     

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.     

Effect of sumatriptan, a 5HT1 agonist, on the frequency of transient lower esophageal sphincter relaxations and gastroesophageal reflux in healthy subjects

OBJECTIVE: Meals increase the rate of transient lower esophageal sphincter (LES) relaxations, in part by gastric distension. The 5HT1 agonist sumatriptan reduces fasting fundic tone, prolongs the meal-induced fundic relaxation, and delays gastric emptying. We therefore hypothesized that sumatriptan might have a significant effect on the rate of postprandial transient LES relaxations and gastroesophageal reflux. We aimed to study the effect of sumatriptan on postprandial transient LES relaxations and reflux in healthy subjects. METHODS: Esophageal manometry and pH monitoring were performed in 13 healthy volunteers for 30 min before and 90 min after a semiliquid meal (790 kcal). Sumatriptan 6 mg subcutaneous (s.c.) or s.c. placebo were administered on separate days 30 min after the meal. RESULTS: Sumatriptan significantly increased postprandial LES pressure from 11.0 +/- 1.2 mm Hg to 17.6 +/- 1.2 mm Hg (p < 0.05). However, reflux events were not diminished. In the contrary, reflux was more frequent after sumatriptan than after placebo (3 [1.5-4.5]/30 min vs 2 [0-3]/30 min, p < 0.05). Transient LES relaxations were more frequent after sumatriptan, particularly in the second 30-min period after drug administration (3 [2.5-5]/30 min vs 2 [1.5-2]/30 min, p < 0.05). CONCLUSIONS: Sumatriptan prevents the natural decay in rate of transient LES relaxations that occurs after a meal and favors the occurrence of gastroesophageal reflux despite increasing LES pressure. The sustained postprandial high rate of transient LES relaxations after sumatriptan may be a consequence of a prolonged fundus relaxation and retention of meal in the proximal stomach.     

Effect of an oral beta2-adrenergic agonist on lower esophageal sphincter pressure in normals and in patients with achalasia

The effect of the beta₂-adrenergic agonist, carbuterol, was studied on the lower esophageal sphincter (LES) pressure in normals and in patients with achalasia. In normals, the mean LES pressure decreased from 23.1±6.2 mm Hg (mean±sem) to 16.0±5.0 mm Hg at a 4.0-mg dose of carbuterol (P<0.05). In patients with achalasia, the mean LES pressure decreased from 50.1±5.1 mm Hg to 22.7±2.4 mm Hg after a 4.0-mg dose of carbuterol (P<0.01). The duration of action following oral administration exceeded 90 min. These studies indicate that the LES in man has beta₂-adrenergic receptors that mediate a reduction in pressure. The magnitude of LES pressure reduction in patients with achalasia suggests that this drug may be of therapeutic benefit.     

Effects of a pH electrode across the lower esophageal sphincter

Recent studies have suggested that combined monitoring of the esophagus and stomach for prolonged periods may be the best method for investigating patients with upper gastrointestinal complaints. However, the effects of an electrode across the LES on esophageal reflux parameters have not been extensively studied. We studied 10 healthy volunteers and 10 patients with GERD twice with 24-hr pH monitoring. In phase 1, two glass electrodes were placed 1 cm below the UES and 5 cm above the LES. One week later in phase 2, patients were restudied with one electrode 5 cm above and one 5 cm below the LES. Although total acid exposure remained the same in healthy volunteers, three volunteers who spontaneously refluxed at night had abnormal prolongation of their supine acid exposure during phase 2 of the study. In patients with GERD, the electrode across the LES resulted in significant (P=0.01) increase in supine acid exposure and showed a strong tendency for the number of reflux episodes >5 min supine (P=0.02) and longest reflux episode supine (P=0.06) to increase without a change in the number of reflux episodes. In conclusion, a small glass electrode across the LES results in prolongation of supine acid exposure in both healthy volunteers spontaneously refluxing at night and the majority of patients with GERD. This results from the electrode interfering with clearance of refluxed acid in the supine position. Thus, combined esophageal and gastric pH monitoring may have important limitations in investigating gastroesophageal symptoms.     

Mean pressure obtained by modified rapid pull-through technique used to assess lower esophageal sphincter function

Lower esophageal sphincter pressure, length of sphincter, and contraction of the crural diaphragm are determinants of esophageal function. Mean pressure manometrics in modified rapid pull-through reflects these three factors. Reproducibility and interobserver variability were studied to assess this method's efficacy and were compared with the maximum expiratory pressure in station pull-through in 44 individuals divided into three groups: achalasia, gastroesophageal reflux, and healthy volunteers. Mean pressure in rapid pull-through showed high reproducibility, no significant differences (14.4 ± 8.4 vs 12.6 ± 8.2 mm Hg) between two measurements, and a high correlation coefficient (r = 0.9). Interobserver variability was lower than that seen for maximum expiratory pressure (P < 0.001). Mean pressure was lower than maximum expiratory pressure in patients with achalasia (21.1 ± 7 vs 30.7 ± 8.6 mm Hg). Both methods showed identical sensitivity to establish a hypotensive sphincter in patients with reflux (73%). We think that mean pressure obtained by rapid pull-through is a good methodology to assess lower esophageal sphincter competence. It is rapid, simple, shows good reproducibility and low interobserver variability, and is clinically valid.     

The role of transsphincteric pressure and proximal gastric volume in acid reflux before and after fundoplication

BACKGROUND & AIMS: This study was conducted to explore the role of proximal gastric volume and transsphincteric pressure on acid reflux during transient lower esophageal sphincter relaxation (TLESR) in patients with gastroesophageal reflux disease (GERD) both before and after laparoscopic fundoplication. METHODS: Twenty GERD patients were studied before and after fundoplication along with 20 healthy controls. High-resolution manometry and pH recording was performed for 1 hour before and 2 hours following meal ingestion (500 mL/300 kcal). Three-dimensional ultrasonographic images of the stomach were acquired before and every 15 minutes after meal ingestion. RESULTS: Postprandial proximal to total gastric volume distribution ratios were significantly larger in GERD patients before fundoplication (0.57 +/- 0.01; P < .05) and smaller following fundoplication (0.37 +/- 0.01; P < .001) compared with controls (0.46 +/- 0.01). The percentage of TLESRs associated with acid reflux did not relate to proximal gastric volume in any subject group. The transsphincteric pressure profile was different for TLESRs with and without reflux in GERD patients as well as in healthy controls. The pressure gradient across the esophagogastric junction (EGJ) (DeltaEGJp) was greater for TLESRs with acid reflux compared with TLESRs without acid reflux in both GERD patients (11.4 +/- 0.8 vs 8.0 +/- 0.5 mm Hg, respectively; P < .01) and controls (10.6 +/- 0.7 vs 7.1 +/- 0.8 mm Hg, respectively; P < .05). After fundoplication, DeltaEGJp during TLESRs was 7.9 +/- 0.9 mm Hg, and the transsphincteric pressure profile markedly changed. CONCLUSIONS: Although proximal gastric volume plays a key role in eliciting TLESRs, it is not related to the incidence of acid reflux during TLESRs. The transsphincteric pressure gradient is greater in TLESRs associated with acid gastroesophageal reflux.     

Effect of Pneumatic Dilation on Gastroesophageal Reflux in Achalasia

The aims of this study were to assess the effectof pneumatic dilation on gastroesophageal reflux inachalasia, differentiate esophageal acid due to lactatefrom acid due to gastroesophageal reflux, and determine if chest pain and heartburn arereliable indicators of gastroesophageal reflux. Eightuntreated achalasia patients underwent pre- andpostdilation esophageal fluid/food residue lactate andpH analysis, esophageal manometry, 24-hr pHmonitoring, and symptom assessment. All patients had asuccessful clinical outcome and a decrease in loweresophageal sphincter pressure from 29.1 ± 12.7 to14.7 ± 3.8 mm Hg (mean ± SD; P = 0.04). Abnormalacid exposure was present in two patients before and twopatients after dilation. Postdilation acid exposure wasmild. Lactate was detected before dilation in allpatients. A lactate concentration 2 mmol/liter wasassociated with acidic residue and one abnormal 24-hr pHprofile. There was no correlation between an abnormal24-hr pH test and age, lower esophageal sphincter pressure, or duration of symptoms prior totreatment. Chest pain and heartburn were unrelated todrops in pH. Gastroesophageal reflux is rare inuntreated achalasia and esophageal acidity may resultfrom ingestion of acidic foods or production oflactate. Mild gastroesophageal reflux occurs afterdilation but is of no clinical significance. Chest painand heartburn are not indicators of acid reflux inachalasia.     

Excess gastroesophageal reflux in patients with hiatus hernia is caused by mechanisms other than transient LES relaxations

BACKGROUND & AIMS: Esophageal acid exposure is higher in gastroesophageal reflux disease (GERD) patients with hiatus hernia than in those without. We investigated the effect of a sliding hiatus hernia on the mechanisms underlying spontaneous gastroesophageal reflux over 24 hours. METHODS: Twelve GERD patients with and 10 GERD patients without hiatus hernia were studied for 24 hours. Combined esophageal pH and manometric recordings of the pharynx, lower esophageal sphincter (LES), and stomach were performed using a multiple-lumen assembly incorporating a Dent sleeve connected to a portable water-perfused manometric system and a pH glass electrode. RESULTS: Patients with hiatus hernia had greater esophageal acid exposure (7.6% vs. 3.3%; P < 0.01) and more reflux episodes (3.1 vs. 1.8/h; P < 0.001) than those without. LES pressure, the incidence of transient LES relaxations (TLESRs), and the proportion of TLESRs associated with acid reflux were comparable in both groups. Both groups had equal numbers of reflux episodes associated with TLESRs and swallow-associated prolonged LES relaxations. Patients with hiatus hernia had more reflux associated with low LES pressure, swallow-associated normal LES relaxations, and straining during periods with low LES pressure. CONCLUSIONS: The excess reflux in GERD patients with hiatus hernia compared with those without is caused by malfunction of the gastroesophageal barrier during low LES pressure, swallow-associated normal LES relaxations, deep inspiration, and straining.     

Achalasia in the elderly

Clinical and manometric data from 13 elderly subjects with idiopathic achalasia (mean age 79±2 years) were compared with findings from younger subjects with the same disease (n=79) to see if aging altered the presentation and outcome of this motor disorder. Fewer elderly subjects complained of chest pain (27% vs 53%), and the pain was significantly less severe (P<0.01). Other presenting features (including sex, duration of symptoms, and presence and severity of dysphagia) did not differ between the groups. Across all patients, age weakly and inversely correlated with residual postdeglutitive lower esophageal sphincter (LES) pressure (R=–0.34), and residual pressure was significantly lower in the older subjects (8.0±1.3 mm Hg vs 11.9±0.8 mm Hg;P=0.02). No differences in basal LES pressure or esophageal-body contraction amplitudes were present between the groups. Initial success with pneumatic dilation was similar in the two subject groups, but the number of older subjects available for analysis was too small to draw strong conclusions. These results indicate that aging decreases the elevation of LES residual pressure that occurs with achalasia. As elderly achalasia patients also present with less chest pain, the findings may be interrelated.Supported in part by grant AMO7130 from the United States Public Health Service. Dr. Todorczuk is supported by an educational grant from Smith, Kline, and French.     

The contribution of the diaphragm and an intrinsic sphincter to the gastroesophageal antireflux barrier. An experimental study in the dog

The components of the mechanical gastroesophageal antireflux barrier were studied in anesthetized dogs (15-18.5 kg). Pressure in the gastroesophageal junction area was recorded by pull-through manometry (using an infused end-hole-provided catheter) during gastric filling (distension) with water. In addition, the gastric volume at which reflux occurred was used as a measure of function and competence. Each dog was studied while intact and spontaneously breathing, after muscle relaxation, after excision of the left half of the diaphragm, and after death. In the intact dogs a barrier with a mean resting pressure of 20 (range, 14-26) cm H2O was recorded. During gastric filling the barrier pressure initially increased to 32 (16-42) cm H2O before steadily decreasing until reflux occurred. The highest pressure was recorded with 625 ml (250-1500 ml) in the stomach. Reflux occurred at a gastric volume of 3200 ml (2300-4000 ml). Muscle relaxation changed neither resting pressure nor reflux volume significantly. After excision of the left half of the diaphragm a barrier with a resting pressure of 15 (6-22) cm H2O was still recorded. Reflux then occurred at a gastric volume of 1400 ml (500-2500 ml). In dead dogs no pressure barrier could be recorded, and reflux was provoked already by 500 ml (250-750 ml) in the stomach. The presence of a mechanical barrier also after excision of the left half of the diaphragm, as evidenced by both pressure and reflux volume, can only be explained by an intrinsic sphincter, a lower esophageal sphincter (LES). However, the experiments also showed that the diaphragm contributed to the competence of the LES. This contribution was at first passive.     

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.     

Lower-esophageal sphincter function does not determine resting upper-esophageal sphincter pressure

Records of 269 esophageal motility studies were reviewed to determine the relationship between lower-esophageal sphincter (LES) function and upper-esophageal sphincter (UES) pressure. Average and greatest UES pressures were similar in patients with LES pressures less than 10 mm Hg or greater than 20 mm Hg, and in patients with and without gastroesophageal reflux as determined by an intraesophageal pH electrode test. Although teliologically appealing, the belief that patients with weak lower-esophageal sphincters and gastroesophageal reflux have stronger upper-esophageal sphincters to guard against pharyngeal reflux and aspiration cannot be confirmed by current manometric techniques.