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.     

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…     

Delivery of radiofrequency energy to the lower oesophageal sphincter and gastric cardia inhibits transient lower oesophageal sphincter relaxations and gastro-oesophageal reflux in patients with reflux disease

Background and aims: Radiofrequency energy (RFe) treatment to the lower oesophageal sphincter (LOS) and gastric cardia is a new luminally delivered therapy proposed as an alternative treatment for gastro-oesophageal reflux disease (GORD). However, it is unclear how RFe achieves its antireflux effect. This study investigated the effects of RFe on mechanisms of spontaneous reflux in patients with GORD. METHODS: Twenty patients with GORD underwent endoscopy, symptom evaluation, and combined postprandial oesophageal manometry and pH monitoring before and six months after RFe, and 24 hour ambulatory pH monitoring before and at six and 12 months after treatment. RESULTS: RFe reduced the rate of postprandial transient LOS relaxations from 6.8 (5.7-8.1) (median (interquartile range) per hour to 5.2 (4.2-5.8) per hour (p<0.01), and increased mean basal LOS pressure from 5.2 (SEM 0.3) mm Hg to 8.0 (SEM 0.4) mm Hg (p<0.01). The number of reflux events was reduced from 10 (2-15.3)/3 hours to 5 (3.5-8.5)/3 hours (p<0.05) and there was an associated significant reduction in acid exposure time from 5.4% (0.4-14.7) to 3.9% (0.4-6.6) (p<0.05). RFe significantly reduced ambulatory oesophageal acid exposure from 10.6% (7.8-13.0) to 6.8% (3.1-9.1) (p<0.01) at six months and 6.3% (4.7-10.9) (p<0.05) at 12 months. All patients required acid suppressant medication for symptom control before RFe. Six months after treatment, 15 patients (75%) were in symptomatic remission and 13 (65%) at 12 months. CONCLUSIONS: RFe has significant effects on LOS function that are associated with improvement in the antireflux barrier. Uncontrolled clinical data also suggest a beneficial effect in the control of reflux symptoms in these patients.     

Cannabinoid receptor agonism inhibits transient lower esophageal sphincter relaxations and reflux in dogs

BACKGROUND & AIMS: Transient lower esophageal sphincter relaxations (TLESRs) are the major cause of gastroesophageal acid reflux, and are triggered by postprandial gastric distention. Stimulation of GABA(B) receptors potently inhibits triggering of TLESR by gastric loads. The functional similarity between GABA(B) and cannabinoid receptors (CBRs) prompted us to study the role of CBRs on mechanisms of gastric distention-induced TLESRs. METHODS: Gastric nutrient infusion and air insufflation was performed during gastroesophageal manometry in conscious dogs. The effects of the CBR agonist WIN 55,212-2 were assessed alone and in combination with the CBR1 antagonist SR141716A or the CBR2 antagonist SR144528. The effects of WIN 55,212-2 were also studied on firing of gastric vagal mechanosensitive afferents in an isolated preparation of ferret stomach. RESULTS: WIN 55,212-2 (57 nmol/kg) inhibited the occurrence of TLESR after gastric loads by 80% (P < 0.01). The latency to the first TLESR after the load was prolonged (P < 0.001), and the occurrence of swallowing was reduced (P < 0.05). The CBR1 antagonist SR141716A reversed the effects of WIN 55,212-2, whereas the CBR2 antagonist SR144528 did not. The CBR1 antagonist alone increased occurrence of TLESR (P < 0.05). The responses of gastric vagal mechanoreceptors to distention were unaffected by WIN 55,212-2 at a concentration of 3 micromol/L. CONCLUSIONS: Exogenous and endogenous activation of the CBR1 receptor inhibits TLESRs. The effects of CBR1 are not mediated peripherally on gastric vagal afferents, and therefore are most likely in the brain stem.     

Pathophysiology of gastroesophageal reflux diseases in Chinese--role of transient lower esophageal sphincter relaxation and esophageal motor dysfunction

BACKGROUND AND AIMS: Transient lower esophageal sphincter relaxation (TLESR) is the major mechanism for gastroesophageal reflux in the Western population. The major reflux mechanism in Chinese patients with GERD has not been studied before. METHODS: Fifty-four patients with GERD and 28 controls underwent stationary baseline manometry and the 24-h ambulatory esophageal pH monitoring. TLESRs were measured before and after an 850 kcal meal in the supine position. Primary peristalsis, secondary peristalsis, and esophageal acid clearance were measured by esophageal manometry. RESULTS: Total time esophageal pH 相似文献   

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.     

Inhibition of transient lower esophageal sphincter relaxation and gastroesophageal reflux by metabotropic glutamate receptor ligands

BACKGROUND & AIMS: Transient lower esophageal sphincter relaxation (TLESR) is the major mechanism of gastroesophageal acid reflux. TLESR is mediated via vagal pathways, which may be modulated by metabotropic glutamate receptors (mGluRs). Group I mGluRs (mGluR1 and 5) have excitatory effects on neurons, whereas group II (mGluR2 and 3) and group III (mGluR4, 6, 7, and 8) are inhibitory. This study determined the effect of mGluRs on triggering of TLESR and reflux in an established conscious ferret model. METHODS: Esophageal manometric/pH studies were performed in ferrets with chronic esophagostomies. TLESR were induced by a gastric load of 25 mL glucose (pH 3.5) and 30 mL air. RESULTS: In control treated animals, gastric load induced 3.52 +/- 0.46 TLESRs per 47-minute study, 89.7% of which were associated with reflux episodes (n = 16). The mGluR5 antagonist MPEP inhibited TLESR dose dependently, with maximal 71% +/- 7% inhibition at 35 micromol/kg (n = 9; P < .0001). MPEP also significantly reduced reflux episodes (P < .001) and increased basal lower esophageal sphincter pressure (P < .05). MPEP inhibited swallowing dose dependently, suggesting a common action on trigger mechanisms for swallowing and TLESR. The more selective analogue, MTEP, had more potent effects (90% +/- 6% inhibition TLESR at 40 micromol/kg; n = 8; P < .0001). In contrast, the group I agonist DHPG tended to increase TLESR. The group II agonist (2R, 4R)-APDC was ineffective, whereas the group III agonist L-(AP4 slightly reduced TLESR (33% at 11 micromol/kg; P < .05). The selective mGluR8 agonist (S)-3, 4-DCPG inhibited TLESR by 54% at 15 micromol/kg (P < .01). CONCLUSIONS: mGluR5 antagonists potently inhibit TLESR and reflux in ferrets, implicating mGluR5 in the mechanism of TLESR. mGluR5 antagonists are therefore promising as therapy for patients with GERD.     

Mechanoreceptors of the proximal stomach: Role in triggering transient lower esophageal sphincter relaxation

BACKGROUND AND AIMS: The role of fundic tension and stretch mechanoreceptors in triggering transient lower esophageal sphincter (LES) relaxation is still unknown. This information would be useful for the development of effective pharmacologic strategies. To elucidate this topic, gastric contractile activity was modified during isovolumetric gastric distention at 2 different volumes. METHODS: LES (Dentsleeve) and gastric (barostat) motility were recorded in 21 healthy subjects during studies comprising two 30-minute isovolumetric gastric distentions (placebo and glucagon or erythromycin). Glucagon (bolus of 4.8 microg/kg plus infusion of 9.6 microg x kg(-1) x h(-1)) was administered at high intragastric volume (i.e., 75% of the threshold volume for discomfort; n = 7) and erythromycin (3 mg/kg) at high (n = 7) and low intragastric volume (i.e., at perception threshold; n = 7). RESULTS: Glucagon decreased (P < 0.05) baseline intragastric pressure and abolished gastric contractions (0 vs. 16.7 +/- 2.3), whereas erythromycin increased (P < 0.05) baseline pressure and doubled (P < 0.05) the rate of gastric contractions at both volumes. Neither drug affected the rate of transient LES relaxations. Low intragastric volume induced a lower rate of transient LES relaxations (1.7 +/- 0.3 vs. 5.7 +/- 1.1; P < 0.01) and gastric contractions (11.8 +/- 2.5 vs. 20.5 +/- 3.1; P < 0.05) compared with high volume but similar baseline intragastric pressure (10.6 +/- 0.6 vs. 11.9 +/- 0.9 mm Hg). CONCLUSIONS: Stretch receptors (gastric volume) seem to be more relevant than tension receptors in triggering transient LES relaxation.     

Effect of prolonged gastric distention on lower esophageal sphincter function and gastroesophageal reflux

OBJECTIVES: Morbidly obese patients treated with an intragastric balloon report a transient increase in gastroesophageal reflux (GER) symptoms. In the present study, we evaluated the underlying mechanisms of GER and examined the effect of prolonged gastric distention on lower esophageal sphincter function. METHODS: Fasting and postprandial manometric studies were performed in obese subjects (n = 15) before, immediately after, and 10 and 20 wk after placement of a 500-ml water-filled balloon. RESULTS: Residual lower esophageal sphincter (LES) pressure after water swallows was not affected after balloon placement, excluding mechanical interaction with sleeve function. Postprandial LES pressure was significantly increased after 10 and 20 wk. GER was increased in the right recumbent position until 10 wk after balloon placement, mainly because of an increased percentage of transient lower esophageal sphincter relaxations (TLESRs) accompanied by GER. TLESRs were the main mechanisms underlying reflux both before and after balloon placement. The rate of TLESRs was increased significantly immediately after introduction of the balloon, returning to baseline values after 20 wk. After balloon placement, reflux episodes were evoked by gastric contractions that were not inhibited by meals. CONCLUSIONS: Chronic distention by an intragastric balloon increased reflux up to 10 wk after placement because of an increase in the percentage of TLESRs accompanied by a reflux episode. In addition, prolonged balloon distention increased the rate of TLESRs and created a postprandial state even 10 wk after balloon placement. After 20 wk these effects largely resolved, illustrating adaptation to this artificial situation.     

Increased frequency of transient lower esophageal sphincter relaxation induced by gastric distention in reflux patients with hiatal hernia

BACKGROUND & AIMS: This study aimed to determine if hiatal hernia influences vulnerability to reflux and transient lower esophageal sphincter relaxation (tLESR) during gastric distention in patients with gastroesophageal reflux disease (GERD). METHODS: Eight normal subjects and 15 patients with GERD were studied. A metal clip attached to the squamocolumnar junction (SCJ) was beneath the hiatus in all control subjects. Eight GERD patients with >/=1-cm SCJ-hiatus separation were considered hernia patients, and 7 with <1-cm separation were considered nonhernia patients. Manometry and esophageal pH were recorded for 30 minutes, after which the stomach was loaded with acid dextrose and the recording continued for 2 hours with intragastric air infusion of 15 mL/min. RESULTS: Baseline reflux was comparable among groups. Gastric distention increased the frequency of reflux by the tLESR mechanism in all groups. Controls and nonhernia patients had median increases of 4.0 and 4.5 in tLESR frequency, respectively, and hernia patients had a median increase of 9.5/h. tLESR frequency was highly correlated with the SCJ-hiatus separation (r = 0.76; P < 0.001). CONCLUSIONS: Gastric air infusion was a potent stimulus for tLESR and reflux. The resultant tLESR frequency was directly proportional to the separation between the SCJ and hiatus, suggesting that the perturbed anatomy associated with hiatal hernia predisposed to eliciting tLESRs in patients with GERD.     

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.     

The lower esophageal sphincter in gastroesophageal reflux in children.

Esophageal function was evaluated in 51 children less than 2 years of age with radiologic evidence of gastroesophageal reflux. Detection of an acid esophageal pH was a sensitive measure of gastroesophageal reflux. Lower esophageal sphincter pressures were greater in reflux patients with respiratory symptoms (18.0 +/- 1.4 mm Hg) than in reflux patients without respiratory symptoms (9.5 +/- 1.0 mm Hg). The intra-abdominal segment of the lower esophageal sphincter was shorter in patients with reflux than in controls (0.51 +/- 0.05 cm vs. 0.75 +/- 0.08 cm). It was also shorter in patients requiring surgical therapy (0.34 +/- 0.05 cm) than in those responding to medical therapy (0.63 +/- 0.07 cm).     

Abolition of gas reflux and transient lower esophageal sphincter relaxation by vagal blockade in the dog

In the present study we have examined the hypothesis that transient lower esophageal sphincter relaxations are under vagal control. Fasting esophageal motor function was monitored with a manometric sleeve catheter passed via a cervical esophagostomy. Gastric insufflation with oxygen resulted in intermittent venting of gas into the esophagus during transient lower esophageal sphincter relaxations. Such venting of gas was associated with the occurrence of esophageal body common cavities and gas venting from the esophageal stoma, all of which increased with increasing rates of gastric insufflation. The optimal insufflation rate, 80 ml/min, produced stomal gas venting at a rate of 10.3 +/- 1.1/h (mean +/- SE). The time and pressure profiles of transient lower esophageal sphincter relaxations induced by gastric insufflation were similar to those relaxations seen with spontaneous postprandial gastroesophageal reflux and belching in dogs. Sphincteric relaxation started 10 s before the onset of common cavities. In all 4 dogs, cooling of cervical subcutaneous vagosympathetic loops abolished transient lower esophageal sphincter relaxations, common cavities, and stomal gas venting. Within 1-4 min of cessation of vagal cooling, all three markers of gastroesophageal gas venting returned. Atropine, 50 and 200 micrograms/kg i.v., did not block transient lower esophageal sphincter relaxations or gas reflux. Gastric gaseous distention is a potent and consistent trigger of transient lower esophageal sphincter relaxations in the dog. This effect can be used as a model for study of control mechanisms of transient sphincter relaxation-dependent gastroesophageal reflux. Our observations with this model indicate that transient lower esophageal sphincter relaxations are under vagosympathetic control, but that muscarinic mechanisms are not important mediators of this control.     

Cholinergic blockade inhibits gastro-oesophageal reflux and transient lower oesophageal sphincter relaxation through a central mechanism

BACKGROUND: Atropine, an anticholinergic agent with central and peripheral actions, reduces gastro-oesophageal reflux (GOR) in normal subjects and patients with gastro-oesophageal reflux disease (GORD) by inhibiting the frequency of transient lower oesophageal sphincter relaxation (TLOSR). AIMS: To compare the effect of methscopolamine bromide (MSB), a peripherally acting anticholinergic agent, with atropine on the rate and mechanism of GOR in patients with GORD. METHODS: Oesophageal motility and pH were recorded for 120 minutes in 10 patients with GORD who were studied on three separate occasions. For the first two recording periods, either atropine (15 microg/kg bolus, 4 microg/kg/h infusion) or saline were infused intravenously. MSB (5 mg orally, four times daily) was given for three days prior to the third recording period. RESULTS: Atropine significantly reduced basal LOS pressure (12.6 (0.17) mm Hg to 7.9 (0.17) mm Hg), and the number of TLOSR (8.1 (0.56) to 2.8 (0. 55)) and reflux episodes (7.0 (0.63) to 2.0 (0.43)) (p<0.005 for all comparisons). MSB reduced basal LOS pressure (12.6 (0.17) to 8.7 (0. 15) mm Hg, p<0.005), but had no effect on the frequency of TLOSR (8. 1 (0.56) to 7.5 (0.59)) and reflux episodes (7.0 (0.63) to 4.9 (0. 60)) (p>0.05). CONCLUSION: In contrast to atropine, MSB has no effect on the rate of TLOSR or GOR in patients with GORD. Atropine induced inhibition of TLOSR and GOR is most likely mediated through a central cholinergic blockade.     

Colonic fermentation influences lower esophageal sphincter function in gastroesophageal reflux disease

BACKGROUND & AIMS: Colonic fermentation of carbohydrates is known to influence gastric and esophageal motility in healthy subjects. This study investigated the effects of colonic fermentation induced by oral administration of fructooligosaccharides (FOS) in patients with gastroesophageal reflux disease (GERD). METHODS: In the cross-over design used in the study, 9 patients with symptomatic GERD were administered a low-residue diet (i.e., 10 g fiber/day) during 2, 7-day periods, receiving either 6.6 g of FOS or placebo 3 times daily after meals. Each period was separated by a wash out of at least 3 weeks. On day 7, esophageal motility and pH were recorded in fasting conditions and after a test meal containing 6.6 g of FOS or placebo. Breath hydrogen concentrations (reflecting colonic fermentation) and plasma concentrations of glucagon-like peptide 1 (GLP-1), peptide YY, and cholecystokinin were monitored. RESULTS: Compared with placebo, FOS led to a significant increase in the number of transient lower esophageal sphincter relaxations (TLESRs) and reflux episodes, esophageal acid exposure, and the symptom score for GERD. The integrated plasma response of GLP-1 was significantly higher after FOS than placebo. CONCLUSIONS: Colonic fermentation of indigestible carbohydrates increases the rate of TLESRs, the number of acid reflux episodes, and the symptoms of GERD. Although different mechanisms are likely to be involved, excess release of GLP-1 may account, at least in part, for these effects.     

Three-dimensional imaging of the lower esophageal sphincter in healthy subjects and gastroesophageal reflux

The resting pressure and intraabdominal length are the most important factors which determine competence of the lower esophageal sphincter (LES). The intraabdominal sphincter vector volume (ISVV) is a single value which takes into account both of these measurements. Normal values of ISVV and of the total sphincter vector volume (TSVV) were established in 20 normal subjects. The sensitivity and the specificity of ISVV and TSVV were then evaluated in 81 patients with gastroesophageal reflux disease (GERD) and in 19 normal subjects and were compared with the usual stepwise pullback manometry (SPM) measuring the resting pressure of the LES at the respiratory inversion point. The motorized pullthrough technique was used to perform the vector volume procedure. Normal values of ISVV were 1870–10740 mm Hg² × mm, and of TSVV 2200–13110 mm Hg² × mm. The sensitivity of ISVV was 93.8% (p < 0.05), of TSVV 80.2%, and of SPM 81.5%. The specificity of ISVV and TSVV was 89.5% and of SPM 78.9% (not significant). Analysis of the intraabdominal sphincter vector volume is more sensitive than the total sphincter vector volume or standard stationary manometry in establishing a defective LES in patients with GERD. Intraabdominal sphincter vector volume analysis will allow surgeons better to identify patients with a defective LES who may be suitable for antireflux surgery.     

Augmentation of lower esophageal sphincter pressure and gastric yield pressure after radiofrequency energy delivery to the gastroesophageal junction: a porcine model

BACKGROUND: An endoscopic technique that eliminates gastroesophageal reflux disease would be of benefit to patients. The endoscopic delivery of radiofrequency energy to the porcine gastroesophageal junction was investigated and its effect on lower esophageal sphincter pressure, gastric yield pressure, and histology was assessed. METHODS: Twenty pigs underwent esophageal manometry and endoscopic injection of botulinum toxin (100 units) into the lower esophageal sphincter. After 1 week, animals were randomized to radiofrequency energy treatment of the gastroesophageal junction with a 4- needle catheter and thermocouple-controlled generator (n = 13) or no further intervention (control, n = 7). At 9 weeks, animals underwent esophagoscopy, manometry, gastric yield pressure determination, and sacrifice for histopathologic evaluation. RESULTS: Mean lower esophageal sphincter pressure declined by 3.7 +/- 2.6 mm Hg (control, p = 0.03) vs. 0.97 +/- 5.8 mm Hg (radiofrequency, p = 0.29) after 9 weeks. Mean gastric yield pressure was 24.9 +/- 8.2 mm Hg (control), compared with 43.4 +/- 10. 7 mm Hg (radiofrequency) (p = 0.0007). Histopathologic assessment demonstrated normal mucosa, mild fibrosis, and no inflammation. CONCLUSIONS: Radiofrequency energy delivery reversed much of the lower esophageal sphincter pressure reduction achieved with botulinum toxin injection and augmented gastric yield pressure by 75% compared with controls. Given the safety of radiofrequency energy delivery in this study and in other areas of medicine, human studies to assess the effect of radiofrequency energy on gastroesophageal reflux disease are warranted.     

Compliance measurement of lower esophageal sphincter and esophageal body in achalasia and gastroesophageal reflux disease

Little is known about the effect of achalasia and gastroesophageal reflux disease (GERD) on compliance of the esophageal body and the lower esophageal sphincter (LES). Twenty-two patients with achalasia, 14 with GERD, and 14 asymptomatic volunteers were assessed. Recording apparatus consisted of a specially developed PVC bag tied to a compliance catheter, a barostat, and a polygraph. Intrabag pressures were increased incrementally while the bag volume was recorded. In each subject, pressure–volume graphs were constructed for both the esophageal body and LES and the compliance calculated. In achalasia, compliance of the esophageal body was significantly higher (P < 0.01) than in controls, whereas LES compliance was similar. Patients with GERD had a highly compliant LES in comparison to both controls and to patients with achalasia (P < 0.01 and P < 0.001, respectively); however there was no difference in their esophageal body compliance. In conclusion, foregut motility disorders can cause changes in organ compliance that are detectable using a barostat and a suitably designed compliance bag. Further measurement of compliance may provide clues to the pathogenesis of these disorders.