Gastric distention: a mechanism for postprandial gastroesophageal reflux

The occurrence of gastroesophageal reflux after meals may be related to an increase in the rate of transient lower esophageal sphincter (LES) relaxations, the mechanisms of which are not understood. We investigated the effects of gastric distention on LES pressure in 16 normal subjects and 17 patients with gastroesophageal reflux disease. Intraluminal pressure was measured in the gastric fundus, LES, and esophageal body with a manometric catheter incorporating a sleeve device. Gastric distention was performed by injecting 0, 250, 500, or 750 ml of air in randomized order into a balloon and maintaining each stimulus for 15 min. Gastric distention did not significantly alter resting LES pressure in either group. During the basal period the rate of transient LES relaxation in the reflux patients (1.1 +/- 0.4 per 15 min) was greater than that in the normal subjects (0.6 +/- 0.1 per 15 min). Gastric distention resulted in a significant threefold to fourfold increase in the rate of transient LES relaxations in both groups. The reflux patients had a significantly greater proportion of complete relaxations (87%) than did the normal subjects (73%). We conclude that gastric distention, by significantly increasing the rate of transient LES relaxations in both normal subjects and patients with gastroesophageal reflux disease, may contribute to the postprandial increase in gastroesophageal reflux.     

Relationship of Intraluminal pH and Pressure within the Lower Esophageal Sphincter

To determine the relationship between lower esophageal sphincter (LES) intraluminal pressure and its intraluminal pH, we studied six healthy volunteers. We recorded intraluminal pressure and pH concurrently using rapid pull-through, slow pull-through, and station pull-through, as well as, rapid push-through and slow push-through techniques. The results showed that LES length was 35 +/- 4 (SE) mm by RPT and 30 +/- 3 mm by SPT. The pressure was maximal in the proximal half of the LES. On rapid pull-throughs, the intraluminal pH rose from about 1.5 to reach a value of about 2.5 at the peak of the high pressure zone. With continued withdrawal into the esophageal body, the recorded pH rose minimally to about 3-4. On push-throughs, the pH recorded along the LES was the same as that of the esophageal body. After the electrode cleared the LES, the pH abruptly fell to gastric pH. During station pull-through with the electrode 0.5-1.5 cm proximal to the distal LES margin, transient pH drops were observed with swallows. With rapid swallows, however, the pH drop did not occur until after the last swallow. This finding suggests that the pH drops with swallows were due to axial LES movement rather than gastroesophageal acid reflux. We conclude that 1) the relationship of the gastroesophageal pH transition zone and LES high pressure zone is better defined by a sphincter push-through than a pull-through; 2) the transition between gastric and esophageal pH occurs either at or slightly distal to the distal LES margin; and 3) swallow-induced axial LES movement may cause spurious recording of acid reflux when the pH probe is positioned within the distal half of the LES.     

Lower esophageal sphincter pressure in normal individuals and patients with gastroesophageal reflux. A comparison between end-hole and side-hole recording techniques

The advantage of a single-lumen end-hole catheter compared with the usual composite side-hole catheter for lower esophageal sphincter (LES) manometry has been studied in vitro and in vivo. In the present study LES pull-through manometry was performed with a special catheter, enabling simultaneous end-hole and side-hole recording of LES pressure. Eighteen normal individuals with normal 24-h pH-monitoring (control group) and 42 reflux patients with pathologic 24-h pH-monitoring (reflux group) were studied. End-hole recorded resting sphincter pressure (RSP) in the control group was 15.4 +/- 5.0 cm H2O and in the reflux group 6.4 +/- 6.4 (p less than 0.0005). Side-hole recorded RSP (mean S1-S3) was 20.8 +/- 11.6 and 11.9 +/- 6.8, respectively (p less than 0.005). End-hole recorded total sphincter length (SL) in the control group was 34 +/- 9 mm and in the reflux group 27 +/- 12 (p less than 0.025) and abdominal sphincter length (ASL) 23 +/- 7 and 16 +/- 9, respectively (p less than 0.005). Side-hole recorded SL was 30 +/- 7 and 30 +/- 12, respectively (NS) and ASL 22 +/- 6 and 18 +/- 9 respectively (NS). After intake of 500 ml of water both LES pressure and length decreased in both groups but the separation between the groups was neither improved nor impaired. The results support the view that LES insufficiency is an important cause of gastroesophageal reflux. That LES had a lower pressure and was shorter in patients with reflux was best demonstrated by end-hole recorded pressure.     

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.     

Relationship of transient lower esophageal sphincter relaxation to postprandial gastroesophageal reflux and belching in dogs

Methods have been developed for the recording of patterns of motor function associated with spontaneous gastroesophageal reflux and belching in trained, unsedated dogs. Pharyngeal, esophageal body, lower esophageal sphincter (LES), and gastric pressures were monitored in 3 dogs with a manometric assembly inserted through a cervical esophagostomy. Spontaneous changes in esophageal pH were recorded simultaneously with a glass electrode. Each dog was studied three times for 3 h starting directly after completion of a full-sized meal. Acid reflux was recorded on 40 occasions; on 35 of these occasions it was possible to analyze, in detail, motor events at the time of reflux. This analysis showed that the LES was completely relaxed at the time of reflux and that the relaxation occurred within the 15 s before the onset of esophageal acidification. In 77% of the reflux episodes LES relaxation occurred independently of swallowing or any other motor event. The remainder of the LES relaxations associated with reflux were secondary to a swallowing salvo or a single swallow that did not trigger an esophageal body peristaltic wave. Straining was associated with reflux during many episodes of LES relaxation, but did not induce reflux if there was measurable LES pressure. Belching was also related to complete LES relaxations with a pattern identical to that associated with acid reflux. In the dog, liquid and gas reflux occurred during transient LES relaxations that were very similar to those that allow reflux to occur in humans. The dog is a suitable model for investigation of the nature and control of reflux associated with transient LES relaxation.     

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.     

Intermittent spatial separation of diaphragm and lower esophageal sphincter favors acidic and weakly acidic reflux

BACKGROUND & AIMS: In small hiatal hernias, the size of the hernia is variable. Intermittent complete reduction can be observed with high-resolution manometry as a transition from a double-peak (hernia) to a single-peak (reduced) high-pressure zone. The aim of this study was to investigate whether intermittent separation of the diaphragm and lower esophageal sphincter (LES) favors the occurrence of gastroesophageal reflux. METHODS: In 16 patients with a small hiatal hernia (3 cm), prolonged high-resolution manometry was performed. Acid and weakly acidic reflux episodes were detected with pH-impedance monitoring. RESULTS: The single pressure peak profile (reduced hernia) was present for 814 minutes (56.5% of total time), and the double peak profile (unreduced hernia) was present for 626 minutes (43.5% of total time). In all patients, both pressure profiles were observed. The transition rate between the 2 profiles was 7.5 +/- 0.9 per hour. More reflux occurred when the LES and diaphragm were separated versus the reduced hernia state (23.1 +/- 5.1 vs 12.2 +/- 2.4 episodes per hour, respectively; P < .05). The proportions of acidic reflux episodes during the single and double pressure peaks were similar (70% and 67%, respectively). In the two-pressure-zone state, there was an increase in all reflux mechanisms except transient LES relaxation. CONCLUSIONS: In patients with a small hiatal hernia, intermittent reduction of the hernia occurs frequently. Spatial separation of the diaphragm and LES in the nonreduced state results in a 2-fold increase in acidic and weakly acidic reflux due to mechanisms other than transient LES relaxation.     

Relationship between straining, transient lower esophageal sphincter relaxation, and gastroesophageal reflux in children

OBJECTIVE: Physical straining such as deep inspiration or coughing may induce gastroesophageal reflux (GER) by overcoming feeble lower esophageal sphincter (LES) pressure. The role of straining as a provocant of GER has not been analyzed systematically in children. It was our aim to examine the contribution of straining to the occurrence of GER with particular attention to its relationship to transient LES relaxations, which are a major mechanism of the occurrence of GER in pediatric patients. METHODS: Concurrent esophageal manometry and pH monitoring was performed for 4 h postprandially in six children with esophagitis (age 9 months to 12 yr). Analysis was performed on isolated single strain episodes, defined as an increased intragastric pressure > 10 mm Hg. When a drop of esophageal pH < 4.0 was noted within 15 sec after any part of a strain, this strain was defined as related to the reflux episode. RESULTS: The median value of basal LES pressure was 10 mm Hg (range 1-18). In all, 134 analyzable strains and 87 analyzable reflux episodes were recorded. Isolated strains were associated with 20 reflux episodes (23%). Reflux was observed more frequently with strains that occurred during transient LES relaxations (12/40) than straining when the LES was contracted (8/94) (p < 0.01). Sustained strain (35%) and inspiratory strain (25%) were the major patterns of straining related to reflux. CONCLUSION: Straining provoked reflux infrequently and simultaneous occurrence of straining and transient LES relaxation was important in determining the occurrence of strain-related reflux in pediatric patients with reflux esophagitis.     

Improved lower esophageal sphincter manometry: application of the end-hole recording technique in vivo

The recommendation to use a thin end-hole catheter for lower esophageal (LES) manometry has a strong theoretic background supported by previous in vitro studies. The pressure in the closed sphincter is measured, and the problem of pressure asymmetry eliminated. In this study the advantage and applicability of an end-hole catheter compared with the composite side-hole catheter for LES manometry was tested in vivo in dogs and human subjects. Pull-through manometry was performed with a continuously infused composite four-lumen catheter with one central channel and three side-hole channels enabling simultaneous end-hole and side-hole recording of LES pressure. A pull-through produced one end-hole and three side-hole pressure registrations. The end-hole recorded resting sphincter pressure was 19.7 +/- 4.5 cm H2O in 6 dogs and 9.9 +/- 6.8 cm H2O in 89 human subjects (volunteers and patients). The side holes recorded higher pressures, longer high-pressure zones, and obvious differences--asymmetry--between the three channels. The correlation between the side-hole and end-hole recordings was equally poor with regard to both pressure and length, with r values from 0.48 to 0.61. The relative difference between the end hole and side holes was most pronounced in low-pressure sphincters. In the dogs the end-hole and one side-hole channel always recorded LES pressure close to the expected 0 pressure during reflux, whereas the other two side-hole channels recorded high pressures. The present study proved the applicability of the end-hole technique for LES manometry in vivo in man. The end hole seemed to record true sphincter pressure.     

Provocation of transient lower esophageal sphincter relaxations by meals in patients with symptomatic gastroesophageal reflux

The effect of a meal on the rate of transient lower esophageal sphinter (LES) relaxations and patterns of gastroesophageal reflux was investigated in 49 patients referred for evaluation of gastroesophageal reflux. Esophageal motility and pH were recorded concurrently before and after a standard meal. In the patients with symptomatic reflux, the meal induced a four-to sevenfold increase in the gastroesophageal reflux through two mechanisms: a four-to fivefold increase in the rate of transient LES relaxations and an increase in the proportion of transient LES relaxations accompanied by reflux from 47% to 68^. Overall the rate of reflux episodes that occurred by mechanisms other than transient LES relaxation did not increase significantly. An exception to these findings were those in six patients with chronically absent basal LES pressure in whom transient LES relaxations could not be scored. In these patients, reflux increased postprandially through mechanisms other than transient LES relaxation. These findings confirm the pivotal importance of transient LES relaxations in the pathogenesis of gastroesophageal reflux.     

酸袋在反流性食管炎中作用的研究

目的 探讨酸袋在反流性食管炎中的作用.方法 应用胃食管反流病问卷(RDQ量表)和胃镜检查确诊15名健康者和24例反流性食管炎患者.使用4通道食管测压系统确定受试者下食管括约肌(LES)位置,将单通道pH电极置于LES远端下方1 cm处监测空腹pH值o.5 h,给予标准餐后继续监测pH值2 h,然后将探针移至LES近端上方5 cm处行24 h动态pH临测.结果 16例反流性食管炎患者(66.67%)与10名健康者(10/15)存在酸袋.反流性食管炎组较健康组酸袋出现时间早[11.00(4.25～17.00)min比30.00(15.50～54.25)min,P＜0.05]、平均pH值低[1.84(1.59～2.19)比2.32(1.96～2.71),P＜0.05].而餐前胃食管连接部平均pH值及酸袋持续时间差异无统计学意义.结论 反流性食管炎患者有异常食管酸反流,且酸袋出现时间早、平均pH值低,其食管黏膜损伤可能与此有关.     

Thoraco-Abdominal Pressure Gradients During the Phases of Respiration Contribute to Gastroesophageal Reflux Disease

Background and Aims  

Exaggerated pressure fluctuation between the thorax and abdomen during exercise or with pulmonary disease may challenge the gastroesophageal barrier and allow reflux of gastric juice into the esophagus. The aim of this study was to investigate the pressure differentials in the region of the gastroesophageal junction to better understand the relationship between the thoraco-abdominal pressure gradient and the lower esophageal sphincter (LES) barrier function.     

Cigarette smoking and gastroesophageal reflux disease.

Proposed pathophysiologic mechanisms relating gastroesophageal reflux disease to cigarette smoking are reviewed. Acute experiments have shown that smokers have chronically diminished lower esophageal sphincter (LES) pressure and that periods of smoking are associated with an increased rate of reflux events. Reflux occurred primarily by the 'abdominal strain mechanism' rather than by transient LES relaxation. Smoking also caused chronically diminished salivary function that results in prolonged acid clearance time. Thus, smoking potentially increases esophageal acid exposure, both by increases in the number of reflux events, and a prolongation of the esophageal acid clearance time.     

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.     

Provocation of transient lower esophageal sphincter relaxations by gastric distension with air

OBJECTIVES: Transient lower esophageal sphincter relaxations (TLESRs) are the major mechanism permitting not only gastroesophageal reflux but also venting of air from the stomach. Triggering of TLESRs is provoked by gastric distension. Antireflux surgery is associated with impaired ability to belch. It is not known whether a reduced capacity to belch results from postoperative reduction in TLESRs. METHODS: We studied the occurrence of TLESRs, common cavities (indicator for gas gastroesophageal reflux), and belching after standardized acute gastric distension by air insufflation (750 ml). Control subjects (n = 10), patients with gastroesophageal reflux disease (GERD) (n = 22), and patients after fundoplication (n = 24) were studied. LES and esophageal motilities were recorded with perfusion manometry. RESULTS: Gastric distension with air significantly (p < 0.05) increased TLESR frequency in controls (1.6+/-0.3 to 3.5+/-1.0 per 20 min), GERD patients (1.2+/-0.3 to 3.1+/-0.5 per 20 min), and patients after fundoplication (0.5+/-0.1 to 1.8+/-0.6 per 20 min). Postfundoplication the number of TLESRs was significantly reduced (p < 0.05) both under fasting conditions and after air insufflation. The number of common cavities and belches after gastric air distension also was significantly reduced (p < 0.05) after fundoplication: 2.3+/-0.6 versus 4.7+/-0.4 in controls and 4.1+/-0.4 in GERD patients. About half of the common cavities occurred during TLESRs, and half during other mechanisms. An impaired ability to belch in daily life correlated with an impaired belching response during the test. An impaired ability to belch occurred only in patients with complete fundoplication and not in patients with partial fundoplication and was associated with a reduced number of common cavities after gastric air insufflation. CONCLUSIONS: Short-lasting gastric air distension 1) provokes TLESRs but does not differentiate GERD patients from controls, 2) reveals impaired belching capacity in patients after complete fundoplication, and 3) shows that common cavities do not exclusively occur during TLESRs.     

Acid-induced esophageal shortening in humans: a cause of hiatus hernia?

BACKGROUND: Hiatus hernia and gastroesophageal reflux disease commonly coexist, and there is pathophysiological evidence that the presence of a hiatus hernia contributes to abnormal acid reflux. However, the cause of hiatus hernia remains unclear. In an animal model, it has been shown that acute acid injury to the esophagus results in esophageal shortening, raising the possibility that reflux esophagitis per se can contribute to the formation of hiatus hernia by inducing esophageal shortening. AIM: To determine whether luminal acid produces esophageal shortening in humans. METHODS: Twelve volunteers were each studied on two occasions, one week apart, in a double-blind, crossover trial. The location of the lower esophageal sphincter (LES), as well as the LES resting pressure and axial length were determined at baseline and then again after 20 min of either acid or saline perfusion. RESULTS: Acid perfusion did not induce significant changes in resting LES pressure but resulted in proximal migration of the LES (ie, esophageal shortening) by an average of 0.5 cm, with the largest proximal migration being 1.8 cm. In contrast, saline perfusion resulted in slight distal migration of the LES (ie, esophageal lengthening). CONCLUSIONS: Intraluminal acid perfusion causes longitudinal axis shortening of the esophagus and suggests that gastroesophageal acid reflux may contribute to the cause of hiatus hernia.     

Acid and duodenogastroesophageal reflux after esophagectomy with gastric tube reconstruction

OBJECTIVE: Patients who undergo esophagectomy with gastric tube reconstruction incur increased risk for acid reflux and duodenogastroesophageal reflux. Few postesophagectomy studies of gastroesophageal reflux disease have included simultaneous 24-h pH and bilirubin monitoring. The aim of this study is to evaluate acid reflux and duodenogastroesophageal reflux after esophagectomy with gastric tube reconstruction. METHODS: Reflux symptom evaluation, endoscopy, and simultaneous 24-h pH and bilirubin monitoring in the cervical esophagus were performed in 25 patients who underwent Ivor Lewis esophagectomy, intrathoracic esophagogastrostomy, and digital dilation of the pyloric ring as treatment for esophageal cancer. RESULTS: Reflux symptoms were severe, mild, and absent in 2, 7, and 16 patients, respectively. Reflux esophagitis and Barrett's esophagus was observed in 11 and 1 patients, respectively. Elevated acid reflux occurred in 7 patients (28%). Elevated duodenogastroesophageal reflux was recorded in 11 patients (44%). Reflux profile analysis identified three patterns: 4 subjects (16%) with both elevated acid reflux and duodenogastroesophageal reflux; 3 (12%) with only elevated acid reflux; and 7 (28%) with only elevated duodenogastroesophageal reflux. Of 7 patients with only elevated duodenogastroesophageal reflux, 4 developed reflux esophagitis. Although reflux symptoms did not correlate with endoscopic esophagitis, a significant correlation was observed between endoscopic esophagitis and acid reflux and/or duodenogastroesophageal reflux. CONCLUSIONS: Reflux symptoms represented a poor indication of esophagitis in patients with esophagectomy and gastric tube reconstruction. Simultaneous 24-h pH and bilirubin monitoring can help in identifying patients at high risk for reflux esophagitis, as well as indicating the cause of esophagitis.     

New observations on the gastroesophageal antireflux barrier

The use of high-frequency ultrasound transducers combined with manometry in the gastrointestinal (GI) tract has yielded important findings concerning the anatomy, physiology, and pathophysiology of the high-pressure zone of the gastroesophageal junction and the sphincteric muscles within. These transducers have made previously invisible portions of the GI tract accessible to investigation. Three distinct high-pressure zones have been identified and correlated with anatomic structures: the extrinsic sphincter (crural diaphragm) and the two components of the intrinsic sphincter (an upper LES and a lower LES [the gastric sling fiber/clasp fiber complex]). This article discusses the possible underlying pathophysiology of gastroesophageal reflux disease; the biomechanics of the gastroesophageal junction high-pressure zone; and the mechanism of action of standard surgical and newer endoscopic therapies for gastroesophageal reflux disease.     

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.     

Antireflux surgery for symptomatic gastroesophageal reflux

To determine the effects of Nissen fundoplication upon the symptoms of reflux and the diagnostic tests employed to evaluate reflux and to examine the relationship between gastroesophageal reflux and lower esophageal sphincter pressure before and after fundoplication, 10 patients with symptomatic reflux were studied before and after operation. Clinical evaluation, barium esophagography, endoscopy with mucosal biopsy, esophageal manometry, acid-perfusion and acid-reflux testing, and gastroesophageal scintiscanning were performed on each patient before and after surgery. Following fundoplication, marked symptomatic, radiographic, endoscopic, and histologic improvement was observed. Serial acid-reflux tests at increasing gastroesophageal pressure gradients returned to normal after surgery. Lower-esophageal-sphincter (LES) pressure increased from 8.2±1.3 to 12.0±1.5 mm Hg (P<0.01). In addition, surgery resulted in a significant decrease in the gastroesophageal reflux index from 17.4±2.4 to 2.7±1.1% (P<0.001). Surprisingly, the pre- and postoperative resting LES pressures did not correlate significantly with corresponding gastroesophageal reflux indices for individual patients. We conclude that increased LES pressure alone does not explain adequately the functional and clinical improvement which follows fundoplication.