Lower esophageal sphincter pressure as an index of gastroesophageal acid reflux

The purpose of this study was to determine the relationship of lower esophageal sphincter (LES) pressure and the volume of acid placed into the stomach required to induce gastroesophageal reflux in man. LES pressure was recorded continuously and by station pull-through by three radially oriented catheters in both symptomatic and asymptomatic subjects during the graded infusions of 0.1 N HCl acid into the stomach. Sumptomatic subjects had a mean LES pressure of 7.5±0.7 mm Hg and refluxed at a volume of 140.0±21.0 ml. Fifty-five percent of asymptomatic subjects refluxed at a mean volume of 380.0±24.7 ml, and had a mean LES pressure of 13.8±0.4 mm Hg. Asymptomatic nonrefluxers at a volume of 500 ml of 0.1 HCL acid had a mean LES pressure of 18.9±1.1 mm Hg. The mean LES pressure and acid volumes showed statistical significance between the three groups (P<0.01). There was an excellent overall correlation between LES pressure and acid volume required to produce reflux in all subjects (r=0.91,P<0.001). Following reflux, asymptomatic but not symptomatic subjects showed a significant increase in LES pressure. These studies suggest that: (1) LES pressure does provide an accurate index of the gastroesophageal antireflux mechanism, provided that acid volume is considered; and (2) asymptomatic subjects showing acid reflux have higher LES pressures, reflux at higher volumes, and develop an LES contractile response after the reflux episode.This work was supported by a grant from the Smith Kline & French Laboratories, Philadelphia, Pennsylvania.     

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.     

Deglutitive pressure responses in the gastroesophageal sphineters of symptomatic hiatal hernia patients

SUMMARY Resting pressures and pressure changes occurring with deglutition were recorded in each 0.5-cm. segment of the gastroesophageal sphincteric zone of 25 patients who had small, symptom-producing, sliding hiatal hernias. Pressures were detected by a water-filled balloon and laterally notched, water-filled polyethylene tubes attached to extracorporeal transducers and measured at end-expiration and end-inspiration. Mean maximal resting pressures in the sphincter were 10.5 cm. of water above gastric pressure (open-tip) and 21 cm. (balloon).With swallowing, a pressure decline below resting tone, indicating relaxation of subhiatal sphincteric segments, was often less pronounced than in health; slight increases occurred frequently. Contraction exceeded relaxation at the hiatus, a reverse of the findings in health. Contraction was most marked above the hiatus while relaxation became progressively less.Despite low resting sphincteric pressure (which probably predisposes to gastroesophageal reflux), impairment of the ability of the sphincter to relax, in addition to increases above resting tone in its subhiatal segments after deglutition, may produce an element of functional obstruction in some symptomatic hiatal hernia patients.Motor dysfunction of the body of the esophagus was frequent: 14 of the 25 patients studied exhibited severe or moderate derangements of contraction.Supported by Research Grant A-4097 from the National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Md.An abstract of a portion of this material was published inClinical Research, December 1963.     

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.     

Effects of exogenous secretin on pancreatic and biliary ductal and sphincteric pressures in man demonstrated by endoscopic manometry and correlation with plasma secretin levels

An endoscopic manometric technique was used to investigate the effects of exogenous secretin on pancreatic duct, common bile duct, pancreatic duct sphincter, and bile duct sphincter pressures in 20 healthy volunteers. Synthetic secretin was infused intravenously at rates of 8.05, 16.1, 32.2, 64.4, 129, 258, and 516 ng/kg/hr, and plasma secretin concentrations were measured by a radioimmunoassay. Secretin produced a significant fall in peak and trough pancreatic duct sphincter pressures from basal values of 48.2±7.9 mm Hg (mean±sd) and 16.9±7.7 mm Hg, respectively, to 34.4±6.8 mm Hg and 11.2 ±5.8 mm Hg (P<0.005), respectively, at a mean plasma secretin concentration of 16 pg/ml (during an infusion rate of 32.2 ng/kg/hr). Higher infusion rates had no additional effect. Pancreatic duct pressure became significantly elevated above basal (11.5±4.0 mm Hg) at the two highest secretin rates. Secretin had no effect on common bile duct or bile duct sphincter pressures. Plasma secretin concentrations were within the postprandial range during the lowest four secretin infusion rates. We conclude that secretin produces selective physiological relaxation of the pancreatic duct sphincter.This work was supported by grants from the Katherine Gavriluk and Sara Jordan Funds, New England Baptist Hospital, Boston, Massachusetts; NIH Research Grant AM 25962. Dr. Carr-Locke is also in receipt of grants from the Wellcome Research Travel Fund, London, England, the Leicester Area Health Authority, Leicester, England, and the P&C Hickinbotham Trust, Leicester, England.     

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.     

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.     

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.     

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.     

Esophageal body and lower esophageal sphincter function in healthy premature infants

Gastroesophageal reflux is a common problem in premature infants. The aim of this study was to use a novel manometric technique to measure esophageal body and lower esophageal sphincter pressures in premature infants. Micromanometric feeding assemblies (OD, ≤2 mm) incorporating 4–9 manometric channels were used in 49 studies of 27 premature neonates. Esophageal body motility was recorded at three sites for 20 minutes after feeding. Twenty attempts (one per minute) were made to stimulate swallowing via facial stimulation (Santmyer reflex). In 32 studies, lower esophageal sphincter pressures were recorded (sleeve) for 15 minutes before and after feeding. Peristaltic motor patterns were less common than nonperistaltic motor patterns (26.6% vs. 73.4%; P < 0.0001) that comprised 31.1% synchronous, 34.6% incomplete, and 6.3% retrograde pressure waves. Reflex swallowing was elicited more frequently in neonates older than 34 weeks postconceptional age than in younger infants (33.4% vs. 20.4%; P < 0.05). Mean lower esophageal sphincter pressure was 20.5 ± 1.7 mm Hg before and 13.7 ± 1.3 mm Hg after feeding (P < 0.0005). Premature infants show nonperistaltic esophageal motility that may contribute to poor clearance of refluxed material. In contrast, the lower esophageal sphincter mechanisms seem well developed.     

A One-Year Follow-up Study of Endoluminal Gastroplication (Endocinch) in GERD Patients Refractory to Proton Pump Inhibitor Therapy

In a subset of patients with gastroesophageal reflux disease (GERD), symptoms persist in spite of proton pump inhibitor (PPI) therapy. Endoscopic gastroplication (EG) was reported to provide a novel therapeutic option in GERD. To evaluate symptomatic and objective outcome of EG in PPI refractory GERD, consecutive GERD patients with persisting reflux symptoms during at least 2 months double dose PPI were recruited for EG (Endocinch). Exclusion criteria were high-grade esophagitis, Barretts esophagus, and hiatal hernia >3 cm. Symptoms and PPI use were evaluated before and 1, 3, and 12 months after the EG; 24-hr pH monitoring off PPI was performed before and after 3 and 12 months. All data are given as mean ± SD and were analyzed by Students t test. Twenty patients (10 females; mean age, 45 ± 11 years) were recruited. Under conscious sedation with midazolam (6 ± 2 mg) and pethidine (53 ± 5 mg), a mean of 2.0 ± 0.2 sutures was applied during a procedure time of 33 ± 6 min. Throat ache and mild epigastric pain for up to 3 days after the procedure were the only adverse events. At 3 and 12 months symptom score (11.6 ± 6 vs. 6.4 ± 3.7 [P < 0.01] and 7.1 ± 4.5 [P < 0.05]) as well as pH monitoring (% time pH < 4: 17.0 ± 1.1 vs. 8.1 ± 5.7% [P < 0.01] and 9.8 ± 4.1% [P < 0.01]) significantly improved. Ph monitoring was normalized (<4% of time) in seven patients after 3 months. PPIs could be stopped in 13 patients, with 2 patients still using H₂-blockers and 1 using cisapride after 3 months. After 12 months only six patients were free of PPI use and pH monitoring was normalized in six patients. We conclude that EG provides short- and medium-term symptomatic and objective relief to a subset of GERD patients refractory to high-dose PPI.     

Identification of Diaphragmatic Crural Component of Gastroesophageal Barrier in the Rat

Manometric assessment of the diaphragmaticcontribution to the human gastroesophageal barrier isdifficult because it overlaps with that of the loweresophageal sphincter. Our aim was to investigate the barrier components in the rat in which thegastroesophageal junction is widely separated from thehiatus. Rats under anesthesia (N = 119) and after musclerelaxation (N = 14) underwent stationary andpull-through perfusion manometry. Inspiratorytransdiaphragmatic pressure gradient was 5.79 ±1.69 mm Hg and lower esophageal sphincter pressure was14.76 ± 8.63 mm Hg. A 13.78 ± 3.13-mmintraabdominal segment of the esophagus was interposed craniallybetween the sphincter and a group of phasic oscillationswith frequency identical to the respiratory rate andpressure of 13.81 ± 6.54 mm Hg, which disappeared after muscle relaxation. Both components of thegastroesophageal barrier in the rat are widely separatedby a long intraabdominal esophagus. This arrangementallows investigation of the behavior of both components under challengingconditions.     

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.     

Pharyngeal swallow in gastroesophageal reflux disease

Outside of the otolaryngologic literature it is not generally recognized that symptoms of gastroesophageal reflux are associated with abnormalities in the larynx and pharynx. Published data of videorecordings of the normal pharyngeal swallow in 16 patients asymptomatic for dysphagia or gastroesophageal reflux were compared to data from recordings from a second group of 70 patients, who were symptomatic for dysphagia or gastroesophageal reflux. Both groups were timed in a similar manner, and the timing data were compared by Studentt-test to determine if functional variations between the groups existed. Fifty-eight timed events occurring during the swallowing process, 23 in the anterior view and 35 in the lateral view, were analyzed. A comparison of events occurring before and after bolus arrival in the esophagus was made. Eighteen percent of events in the pre-esophageal period occurred significantly earlier (p<0.05) in the symptomatic group. Marked differences were seen after the bolus entered the esophagus as 39% of events occurred significantly later in the symptomatic group. Our data suggest that individuals with symptoms of gastroesophageal reflux disease demonstrate a number of functional variations during the pharyngeal swallow. This finding is consistent with structural changes described in the otolaryngologic literature. This study was supported in part by Navy Clinical Investigation Protocol No. 84-06-2038 and USUHS Grant C08900     

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.     

Basal acid output and gastric acid hypersecretion in gastroesophageal reflux disease

The purpose of this study was to evaluate possible differences in basal gastric acid secretion with regard to severity of gastroesophageal reflux disease. Basal acid output was determined by nasogastric suction in 228 patients with gastroesophageal reflux disease who received upper gastrointestinal endoscopy and were diagnosed with either pyrosis alone (N = 98), erosive esophagitis with or without pyrosis (N = 87), or Barrett's esophagus (N = 43). Mean basal acid output for the 228 patients with gastroesophageal reflux disease was 6.5 ± 5.6 meq/hr, which was significantly different from 65 normal subjects with a mean basal acid output of 3.0 ± 2.7 meq/hr (P < 0.0001). Compared to normal subjects, mean basal acid outputs significantly differed for patients with pyrosis (P < 0.05), esophagitis (P < 0.01), and Barrett's esophagus (P < 0.01). There was also a significant difference in mean basal acid output between the patients with pyrosis and Barrett's esophagus (P < 0.01). Nineteen of the 98 patients with pyrosis (19%), 24 of the 87 patients with esophagitis (28%), and 15 of the 43 patients with Barrett's esophagus (35%) had gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr). One hundred forty-six patients with gastroesophageal reflux disease were treated with ranitidine in doses that resulted in complete healing of esophagitis and disappearance of pyrosis. Ninety-three patients responded to ranitidine 300 mg/day; however, 53 patients required increased dose of ranitidine (mean 1205 mg/day, range 600–3000 mg/day). There was a significant correlation between basal acid output and daily ranitidine dose required for therapy for the 146 patients with gastroesophageal reflux disease (r = 0.53,P = 0.0001). Furthermore, a significant association was also found between the presence of gastric acid hypersecretion and the requirement for increased doses of ranitidine (greater than 300 mg/day) (P = 0.00001). These results indicate that there is a subset of patients with gastroesophageal reflux disease who do have idiopathic gastric acid hypersecretion. Moreover, these patients have an apparently higher requirement for medication dosage in order to achieve therapeutic efficacy.     

Reevaluation of manometric criteria for vigorous achalasia

Clinical and manometric data from 97 consecutive patients with idiopathic achalasia were analyzed to see if a distinct subset with vigorous achalasia could be identified. Statistical analyses failed to detect a unique group of subjects based on the distribution of contraction wave amplitudes alone. Because of this, patients falling above the 95th percentile (N=4, mean wave amplitude>100 mm Hg for each) were compared with those having mean amplitudes above the conventional threshold for the diagnosis of vigorous achalasia (mean amplitude 60–100 mm Hg,N=4), and with the remainder (N=89, mean amplitude <60 mm Hg). Subjects with mean amplitudes <60 mm Hg and with mean amplitudes 60–100 mm Hg closely resembled each other in all measured clinical features, whereas subjects with mean amplitudes >100 mm Hg were all male, were older (67±4 years vs 47±2 years; P<0.01), and appeared to have somewhat longer duration of symptoms when compared with the remainder (82±41 vs 44±10 months;P=0.4). Chest pain and other esophageal symptoms, basal and residual lower sphincter pressures, and response to first treatment did not differ among the three groups. These data indicate that high-fidelity manometry techniques identify a rare subset of achalasia patients with mean contraction amplitudes exceeding 100 mm Hg that, although older and possibly with greater duration of symptoms, presents similarly to others with idiopathic achalasia. Outcome from conventional treatment is also similar for the vigorous and nonvigorous patients, making the distinction of questionable value.Supported in part by a grant (AM07130) from the United States Public Health Service. Dr. Todorczuk is supported by a grant from Smith Kline and French.     

Familial clustering of reflux symptoms

OBJECTIVE: A number of case reports describe multiple family members with gastroesophageal reflux disease and Barrett' s esophagus. The wider importance of familial factors in gastroesophageal reflux disease has not been established. Therefore, we have studied the prevalence of reflux symptoms and medication use among relatives of patients with documented gastroesophageal reflux disease. METHODS: A postal questionnaire study of the first degree relatives of six groups of matched patients. The groups comprised patients with 1) no dyspeptic symptoms; 2) reflux symptoms and a normal pH study; 3) reflux symptoms, an abnormal pH study, and a lower esophageal sphincter (LOS) pressure more than 10 mm Hg; 4) reflux symptoms, an abnormal pH study, and a LOS pressure less than 10 mm Hg; 5) Barrett's esophagus; and 6) peptic stricture. RESULTS: Four hundred eighteen subjects replied (78% response). Infrequent reflux symptoms were equally common in all groups of relatives. Frequent reflux symptoms, however, were more common among relatives of patients with an abnormal pH study and normal (26%, p = 0.007) or low LOS pressure (27%, p = 0.01) or Barrett's esophagus (30%, p = 0.003), compared with relatives of nondyspeptic patients (9%). Frequent reflux symptoms were no more common among relatives of patients with a normal pH study (16%) or peptic stricture (18%). Reflux medication use showed a similar pattern. CONCLUSIONS: Familial clustering of reflux symptoms is seen in relatives of patients with reflux symptoms and increased esophageal acid exposure and in relatives of patients with Barrett's esophagus.     

Gastroesophageal Reflux After Combined Lower Esophageal Sphincter and Diaphragmatic Crural Sling Inactivation in the Rat

This study tests the hypothesis that eitherselective or combined destruction of the loweresophageal sphincter and the diaphragmatic crural slingshould induce reflux in the rat. Pull-through perfusion manometry was performed before and after loweresophageal myectomy, crural myotomy, or both. pHmonitoring was used to detect reflux. Unmanipulated ratsserved as controls. Paired t tests were used for comparison of pre- and postoperative pressurevalues and contingency tables with Fisher's tests forexamining the association between the interventions andthe appearance of reflux. Esophageal myectomy decreased only sphincteric pressure from 25.9± 15.5 to 9 ± 6 mm Hg (P < 0.01),whereas crural myotomy decreased only sling pressurefrom 26.2 ± 13.3 to 7.3 ± 3.9 mm Hg (P< 0.01). Simultaneous performance of both procedures decreasedsphincteric and crural pressures from 20.4 ± 7.5to 7.6 ± 4.3 mm Hg (P < 0.01) and from 45.9± 20.6 to 18.2 ± 7.4 mm Hg (P < 0.01),respectively. None of the control, myectomy, or myotomy animalsshowed reflux upon pH-metry but 5/8 rats in which bothprocedures were performed had prolonged acid exposure.No esophagitis was seen. In conclusion, normal rats do not have reflux. Selective destructionof either the sphincter or the crural sling does notinduce reflux, despite causing flattening of theirrespective manometric profiles. Conversely, combined inactivation of both components issignificantly associated with reflux.     

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.