Interdigestive Motor Complex Research Articles

Effect of age on human gastric and small bowel motility.

To test the hypothesis that age alters fasting and postprandial antral and intestinal motility in humans, we studied 23 patients, aged 18-39 years (median 28), and 13 patients, aged 40-69 years (median 49). All were having gastrointestinal symptoms, but in none was there objective clinical, radiologic, or endoscopic features of bowel disease, and manometry of the stomach and proximal small bowel was normal. We quantitated certain parameters of fasting intestinal motility and postprandial antral and jejunal motility. There were no significant differences in the interval between interdigestive motor complexes (IMC), duration, propagation velocity, or maximum number of contractions during phase III of the IMC, or postprandial antral and jejunal motility indices. The postprandial indices show a very similar distribution in each decade. Thus, in selected patients with unexplained gastrointestinal symptoms but no objective features of gut disease, quantifiable gastric and small bowel motility parameters do not differ in the age groups 18-39 and 40-69 years.

Effect of six weeks of treatment with cisapride in gastroparesis and intestinal pseudoobstruction

We have investigated the effect of oral cisapride (10 mg t.i.d.) in a double-blind, placebo-controlled trial in 26 patients with upper gut dysmotility: 11 with gastroparesis (8 diabetic, 3 idiopathic) and 15 with chronic idiopathic intestinal pseudoobstruction. Patients were evaluated at entry and at the end of the 6-wk study by upper gastrointestinal manometry, scintigraphic evaluation of gastric emptying of solids and liquids, measurement of body weight, and scoring of the following symptoms: abdominal pain, nausea, vomiting, early satiety, bloating, and distention. Cisapride and placebo groups were strictly comparable for all parameters assessed. Cisapride resulted in a significant increase in the gastric emptying of solids (p < 0.05) compared with placebo; cisapride also tended to increase the postcibal antral motility and normalize the abnormal manometric features in the patients with intestinal dysmotility, particularly the characteristics of fasting interdigestive motor complexes and the fed motor pattern. Both cisapride and placebo groups showed an improvement in total symptom scores and there was no significant difference in overall symptom response between the two groups. However, the change in abdominal pain was greater with cisapride (p = 0.07). Cisapride facilitates gastric emptying in patients with upper gut dysmotility. The overall symptomatic benefit during a 6-wk trial of cisapride, 10 mg t.i.d., was not greater than that of placebo, and dose-response as well as longer term trials are necessary to determine the clinical efficacy of this medication.

Effect of Six Weeks of Treatment With Cisapride in Gastroparesis and Intestinal Pseudo obstruction

We have investigated the effect of oral cisapride (10 mg t.i.d.) in a double-blind, placebo-controlled trial in 26 patients with upper gut dysmotility: 11 with gastroparesis (8 diabetic, 3 idiopathic) and 15 with chronic idiopathic intestinal pseudoobstruction. Patients were evaluated at entry and at the end of the 6-wk study by upper gastrointestinal manometry, scintigraphic evaluation of gastric emptying of solids and liquids, measurement of body weight, and scoring of the following symptoms: abdominal pain, nausea, vomiting, early satiety, bloating, and distention. Cisapride and placebo groups were strictly comparable for all parameters assessed. Cisapride resulted in a significant increase in the gastric emptying of solids (p less than 0.05) compared with placebo; cisapride also tended to increase the postcibal antral motility and normalize the abnormal manometric features in the patients with intestinal dysmotility, particularly the characteristics of fasting interdigestive motor complexes and the fed motor pattern. Both cisapride and placebo groups showed an improvement in total symptom scores and there was no significant difference in overall symptom response between the two groups. However, the change in abdominal pain was greater with cisapride (p = 0.07). Cisapride facilitates gastric emptying in patients with upper gut dysmotility. The overall symptomatic benefit during a 6-wk trial of cisapride, 10 mg t.i.d., was not greater than that of placebo, and dose-response as well as longer term trials are necessary to determine the clinical efficacy of this medication.

An experimental study of the gastrointestinal motility in conscious dogs with strain gauge force transducers

Interdigestive motor complex (IMC) from the stomach to the ileum and colonic migrating motor complex (CMMC), and the effects of motilin and PYY to them were studied in conscious dogs with strain gauge force transducers (SG). In fasted dogs, IMC cycle times were 100.5 +/- 7.5 min in from the antrum to the ileum and propagation velocity of the small intestine was fastest in the proximal jejunum (4.85 +/- 0.81 cm/min), slowest in the distal ileum (0.81 +/- 0.08 cm/min). The duration of postprandial interruption of motor complex (DIMC) was longer in the antrum and duodenum in 8 dogs of the twelves than the middle and lower intestines. Ileo-colonic propagation rates of IMC that reached to the terminal ileum were 95/116 (81.9%), but the frequency of CMMCs was about 4 times higher than that of IMCs. Each colonic motor complex were classified into four patterns, such as aboral migrating complex (A), oral migrating complex (O), discrete complex (D) and giant migrating contractions (G), and the starting point of migrating complex was marked with -, like A, O or G. Thus, independency index (I I) in each site was defined as: I I = (sum of number of A, O, G and D)/(total number of colonic motor complex). I I was highest in colon 1 (70-80%) and next in colon 4. Motilin (0.5 microgram/kg.hr) elicited IMC like activities in the antrum, duodenum and proximal jejunum, but no effects in the middle and lower small intestine, and the colon. PYY infusion caused dose dependent inhibitions of IMC in the antrum and duodenum, but no effects in the below intestines as same as motilin. These findings suggest that IMCs are basal rhythms of gastrointestinal motility and IMCs occurring from the antrum to the proximal jejunum are more sensitive to the factors as eating or gut peptides.

Abnormal postcibal antral and small bowel motility due to neuropathy or myopathy in systemic sclerosis

Two hypotheses were tested: first, that postcibal motility disorders occur in both the antrum and small bowel of systemic sclerosis patients with gastrointestinal symptoms; second, that dysmotility may result from a neuropathic stage in this disease. Upper gut perfusion manometry (3 h fasting, 2 h fed) was performed and compared with data from similarly studied healthy laboratory controls (n = 15). Only 1 of 8 scleroderma patients had an interdigestive motor complex during the 3-h fasting period [0.1 ± 0.1 (SEM) for systemic sclerosis vs. 1.4 ± 0.16 (SEM) for controls, p < 0.05]; 2 other patients had fasting duodenal incoordinated bursts of phasic pressure activity in the duodenum or proximal jejunum. Distal antral motility index [MI = In (sum of amplitude × number of contractions + 1)] was lower (12.4 ± 0.5, p < 0.01) than that in controls (14.4 ± 0.14); both the amplitude and frequency of antral pressure activity were lower (p < 0.05) in systemic sclerosis. The intestinal fed pattern was characterized by reduced amplitude and frequency of contractions in 6 patients; 2 patients had excessive phasic or tonic small bowel pressure activity, or both. Thus, antral hypomotility is present in most symptomatic scleroderma patients; proximal small bowel postcibal motility is characteristically reduced; a minority of such patients have incoordinated fasting or postcibal hypermotility suggestive of a neuropathy. Manometry identifies the type and region of dysmotility in systemic sclerosis; our results suggest that there are neuropathic and myopathic stages of the upper gut involvement in systemic sclerosis.

24 GASTROINTESTINAL (GI) MOTILITY, DUODENOGASTRIC REFLUX (DGR) AND GASTRIC EMPTYING (GE) IN CHILDREN WITH CHRONIC VOMITING

We evaluated GI motility by means of a perfused catheter system, DGR, as assessed by Bile Salts (BS) output in gastric aspirates, and GE of a milk labeled formula (% of emptying at 1 hr) in 11 patients (pts) with unexplained chronic vomiting. (Apts), in 8 pts with protracted gastroesophageal reflux (GER) disease (Bpts) and in 7 symptomatic controls (Cpts). Mean ± SD age (months) was respectively 44.2±37.7, 18.1±11.2, 20.4±14.4. In 9 Apts and 5 Bpts we found GI manometric abnormalities none of which were seen in Cpts: a) fasting and/or fed antral (and/or duodenal) hypomotility; b) abnormal propagation or configuration of interdigestive motor complexes (IMC); c) bursts of non propagated duodenal or jejunal motility; d) sustained fasting and/or fed phasic activity incoordinated with adjacent gut segments. Both A and B pts had BS fasting recovery significantly higher than Cpts during the various phases of IMC (mean group values (mg/ml): 1.52 (A), 1.12 (B), 0.36 (C), p < 0.05) and a significant delay of GE (A: 32.8±8.9%; B: 34.4±9.8%) as compared to Cpts (64.5±5.3%, p< 0.05, mean±SD). Highest degrees of gastric BS output and of delayed GE were associated with the most marked GI motility dysfunctions in both A and B pts. Conclusions: 1) children with chronic unexplained vomiting may exhibit, at GI manometry, disordered gut motility patterns; 2) the latter seem to be associated with increased DGR and delayed GE; 3) severe GER disease shows diffuse dysmotllity of upper GI tract.

Antroduodenal resistance to flow in the control of duodenogastric bile reflux during fasting

Our objectives in this study were (a) to determine the role of antroduodenal resistance in the control of fasting duodenogastric bile reflux in the dog and (b) to elucidate the contribution of the pylorus both to resistance and to reflux. Thus, we measured simultaneously throughout the interdigestive motor cycle (a) antroduodenal pressure activity by manometry, (b) antroduodenal resistance by a pneumatic resistometer, and (c) bile acid concentrations in duodenal and gastric juices. Experiments were performed in 15 conscious dogs (9 with pylorus intact and 6 with extramucosal pyloric myotomy). We found that antroduodenal resistance was lowest during phase I, increased gradually during phase II, and peaked during phase III (linear trend, p < 0.001). Duodenogastric bile reflux was low during phase I, peaked during late phase II, and decreased again during phase III (quadratic trend, p < 0.05). Therefore, variations in net resistance and reflux were differently related to the phases of the interdigestive motor complex. Pyloric myotomy significantly decreased antroduodenal resistance (linear trend different from control, p < 0.001), but had no significant effect on duodenogastric bile reflux. We conclude (a) that changes in net antroduodenal resistance do not regulate duodenogastric bile reflux and (b) that the pylorus is an important determinant of antroduodenal resistance, but has no major role in the control of fasting duodenogastric bile reflux.

Chronic idiopathic intestinal pseudo-obstruction: clinical and intestinal manometric findings.

We report the clinical and intestinal manometric findings in a group of 42 patients with chronic idiopathic intestinal pseudo-obstruction evaluated at the Mayo Clinic. The main clinical manifestations in these patients were nausea and vomiting (83%), abdominal pain (74%), distension (57%), constipation (36%), diarrhoea (29%), and urinary symptoms (17%). These symptoms preceded surgery in all patients. Air fluid levels or distended bowel loops occurred in 57% and a dilated bladder or urinary excretory pathway in 17%. All patients showed intestinal manometric abnormalities none of which are seen in healthy individuals: aberrant configuration or propagation of interdigestive motor complexes in 25 patients; bursts (greater than 2 min duration) of non-propagated phasic pressure activity in fasting and/or fed state in 30 patients; sustained incoordinated fasting pressure activity in 15 patients; and inability of an ingested meal to convert fasting into fed pattern in 28 patients. We conclude that qualitative analysis of intestinal manometry provides evidence of gut dysmotility in patients with the clinical syndrome of chronic intestinal pseudo-obstruction. These abnormalities of motility can help to establish the correct diagnosis.

Impaired transit of chyme in chronic intestinal pseudoobstruction: Correction by cisapride

Chronic intestinal pseudoobstruction is a clinical syndrome whose pathophysiology, objective diagnosis, and treatment are poorly understood. We investigated 8 patients with this syndrome in whom intestinal dysmotility was established manometrically by two or more of the following criteria: abnormal configuration or propagation of interdigestive motor complexes, sustained incoordinate pressure activity, nonpropagated bursts of phasic pressure activity, and failure of a solid-liquid meal to induce a fed pattern. To establish the functional impairment and region of the gut primarily affected by the disease, we quantified radioscintigraphically the gastrointestinal transit of the solid (131I-fiber) and liquid (99mTc-DTPA) components of a meal. Our techniques allowed us to quantify separately gastric emptying and pylorus-to-cecum transit. Furthermore, we evaluated the effects of a new prokinetic agent, cisapride. Gastric emptying times in pseudoobstruction were not significantly delayed; however, transit times through the small bowel (t1/2) were markedly prolonged [solids, 235 ± 43 min (mean ± SEM) vs. 138 ± 25 controls, p < 0.05; liquids, 310 ± 67 vs. 181 ± 28 controls, p = 0.07]. Cisapride was effective in reducing the delayed intestinal transit time to within the normal range (Δ solids = −115 ± 25 min; Δ liquids = −146 ± 71 min; p < 0.05 for both). These studies suggest that intestinal dysmotility in this group of patients with pseudoobstruction was associated with delayed small bowel transit of radiolabeled solid and liquid components of chyme. Cisapride can restore to normal the delayed transit, indicating that it may potentially correct the impaired propulsive activity in the small bowel of these patients.

Absent postprandial duodenal motility in a child with cystic fibrosis: Correction of the symptoms and manometric abnormality with cisapride

A 19-mo-old boy with cystic fibrosis presented with a lifelong history of feeding problems and constipation, and an 8-mo history of episodes of repeated retching, diaphoresis, dehydration, and somnolence after eating. Tests of esophageal motility and gastric emptying of a 5% glucose meal were normal. Antroduodenal pressure recordings during fasting demonstrated the presence of all phases of the interdigestive motor complex. After consumption of a 240-ml complex liquid meal, however, the contractile pattern that generally accompanies eating was absent and gastric emptying was markedly delayed. When bethanechol or metoclopramide was given 10 min before the complex liquid meal, there was a paucity of contractile activity, gastric emptying was slow, and symptoms of lethargy, diaphoresis, and retching were present. When cisapride was given, there was frequent irregular contractile activity, faster gastric emptying, and no symptoms of lethargy. During the past year treatment with cisapride has been a requirement in order to prevent recurrence of the symptoms. Antroduodenal pressure studies proved helpful in the identification of a treatable manometric abnormality that was associated with symptoms of delayed gastric emptying.

Variations in plasma motilin, somatostatin, and pancreatic polypeptide concentrations and the interdigestive myoelectric complex in dog.

We have looked at the plasma concentrations of motilin, pancreatic polypeptide (PP), and somatostatin (STS) during the various phases of the interdigestive motor complex (IDMC) in dogs. As expected, motilin cyclical increase was always associated with the phase III of the IDMC. Statistical analysis of PP variations revealed a significant rise 10 min before duodenal phase III; however, in individual animals, this relationship was inconsistent. Although a dose-related increase in PP blood levels was induced by administration of synthetic canine motilin (0-200 ng kg-1 iv), fasting plasma levels of PP were not correlated with the concentrations of circulating endogenous motilin. After truncal vagotomy, while motilin release and the intestinal motility pattern remained unaltered, the phase III associated cyclical increases of PP disappeared. Infusion of physiological amounts of PP (1 microgram kg-1 h-1 for 3 h) mimicking the postprandial release failed to reproduce a fed pattern type of intestinal motility and of motilin secretion. No statistical correlation could be established between STS plasma levels and the motor activity of the intestine. STS plasma levels were not correlated with circulating concentrations of motilin and the exogenous administration of physiological doses of synthetic canine motilin failed to modify STS plasma levels. Morphine (200 micrograms kg-1 iv) stimulated only the release of motilin. These data suggest that the role played by circulating concentrations of PP and STS in the control of the IDMC in dog is at most minimal.

Gastrointestinal motility disturbances in patients with orthostatic hypotension

Orthostatic hypotension syndromes may be associated with visceral denervation, resulting in disturbances of the gastrointestinal and urinary systems. This report analyzes the findings in 9 patients with neurogenic orthostatic hypotension and gastrointestinal symptoms. Antral and proximal small intestinal motor dysfunction was demonstrated in all patients: a significant reduction (p = 0.007) in the number of interdigestive motor complexes during 3 h of fasting (mean 0.4 vs. 1.3 controls); absence of gastric component in interdigestive motor complexes observed; incoordination of fasting and fed antral activity; and development of nonpropagating bursts of phase III-like activity in the intestine that were of at least 2-min duration, high amplitude and frequency, and associated with tonic elevations in baseline pressure. These motor abnormalities may provide a potential means for the diagnosis of impaired autonomic supply to the upper gut.

Myoelectric and motor activity of the terminal ileum after pelvic pouch for ulcerative colitis.

The electrical and motor activity of the terminal ileum after proctocolectomy and ileoanal reservoir was evaluated in seven patients who had undergone surgery for ulcerative colitis. Recordings were carried out with an intraluminal probe under fasting conditions, during stepwise distention of the pouch, in the postprandial state and after administration of Prostigmine and bisacodyl. Ileal sensitivity was also studied. Phase III of the interdigestive myoelectric motor complex, when detectable (four patients), was characterized by regular spike bursts superimposed on slow waves at a frequency of 9 cycles per minute. Two different types of motor patterns were observed: short phasic waves lasting 2 to 6 seconds and long tonic waves lasting up to 2 minutes. In most cases, the amplitude and frequency of the pressure events were higher in the efferent limb than in the reservoir. Electrical activity of the surrounding rectal muscle and striated sphincters was also recorded. When distended to the maximum tolerable volume, the reservoir showed spike bursts propagated aborally at a frequency of 15 per minute, leading to large propulsive waves. An overall increase of spike activity was observed after a meal, which did not affect the slow waves. Neostigmine caused an irregular increase of electrical and motor activity, more evident in the efferent limb. Bisacodyl, used to test the functional integrity of the myenteric plexus, elicited strong propulsive contractions and urgency. Leakage did not occur frequently either at rest or under stimuli. Onset of sensation was elicited with volumes of 271 +/- 149 ml (Mean +/- SD) in the reservoir and 17 +/- 6 ml in the efferent loop of small bowel (P less than 0.001). 1) most of the electrical and motor properties of the terminal ileum are retained after surgery; 2) due to its large capacity, the reservoir acts as a storage organ; and 3) overall motility is reduced in the pouch when compared with the distal ileum and propulsion in the triple-loop system is opposed by the activity of the anal sphincters.

Effects of cimetidine and ranitidine on interdigestive and postprandial lower esophageal sphincter pressures and plasma gastrin levels in normal subjects

The purpose of this study was to investigate the effects of cimetidine and ranitidine on human lower esophageal sphincter pressure (LESP) and plasma levels of gastrin in all phases of the interdigestive motor complex and after a test meal. In a random, double-blind manner, placebo, cimetidine (1.0 mg/kg · h), and ranitidine (0.16 mg/kg · h) were administered by intravenous infusion to nine healthy volunteers. By using a sleeve catheter assembly, LESP was constantly monitored, as were esophageal, fundic, antral, and duodenal pressures. Considerable minute-to-minute and interdigestive motor phase-related LESP variations were observed. Cimetidine and ranitidine decreased the interdigestive LESP, but did not abolish the gradual increase in LESP from phase I to phase III. During the first 2 h after the meal, cimetidine and ranitidine had no significant effect on LESP. Plasma gastrin levels were increased by cimetidine and ranitidine, both in the interdigestive and in the postprandial state. The results indicate that the effect of H2-blockers on LESP is not gastrin-mediated. The results further indicate that, in studies on the effects of drugs on LESP, prolonged recording of LESP in all motor states is a prerequisite.

DIFFERENT ACTIONS OF INTRAVENOUS ETHANOL ON BASAL (= INTERDIGESTIVE) SECRETION OF GASTRIC ACID, PANCREATIC ENZYMES AND BILE ACIDS AND GASTROINTESTINAL MOTILITY IN MAN

The action of an intravenous infusion of ethanol (10% v/v; given in a dose of 300 mg kg-1 body weight for 30 min followed by 3 mg kg-1 min-1 for 2 hr) on the basal (= interdigestive) gastrointestinal motor activity and the basal gastric acid, pancreatic amylase and bile acid secretion was determined in 6 healthy human volunteers. Ethanol did not affect the duration of the interdigestive motor complex and the output of bile acids into the duodenum. Ethanol significantly (P less than 0.05) stimulated the gastric acid output by about 2.2-fold and inhibited the pancreatic amylase output by about 43% as compared to control experiments in which an intravenous infusion of 0.15 M NaCl was given. Ethanol did not alter the mean plasma levels of gastrin and pancreatic polypeptide as compared to prestimulatory values and to control experiments. In conclusion, these results show that intravenous ethanol given in a moderate dose stimulates gastric acid output and inhibits pancreatic amylase output in fasting non-alcoholic human beings. The mechanism(s) of these different actions of ethanol is unknown since release of gastrin or pancreatic polypeptide by ethanol does not account for the observed effects of intravenous ethanol.

Effect of traumatic spinal cord transection on human upper gastrointestinal motility and gastric emptying

Whether transection of the spinal cord, above the level of the sympathetic outflow to the gastrointestinal tract, alters human upper gastrointestinal function is yet unknown. In 5 patients with complete high-cord transection (neurologic level above T1), 3 patients with complete low-cord transections (neurologic level T10 or below), and 4 age- and sexmatched healthy controls, the duration of the phases and cycle length of the interdigestive motor complex were similar. However, the percentage of phase III's of the interdigestive motor complex that originated in the antrum and propagated to the duodenum was significantly decreased in patients with high-cord transections compared with healthy subjects (38% vs. 90%; p < 0.05), but was similar in patients with low-cord transections and normal controls (75% vs. 90%). After liquid meals, 3 of the 3 high-cord patients tested had reduced cumulative gastric emptying at 60 min postprandially compared with healthy subjects. Thus, interruption of the cervical cord above the level of the sympathetic outflow to the gastrointestinal tract disturbs normal interdigestive antral-duodenal motor coordination and may delay postprandial gastric emptying of liquid meals.

Interdigestive gastrointestinal motility and secretion of gastric acid and pancreatic enzymes in young cigarette smokers.

The basal (interdigestive) gastrointestinal motor activity and the interdigestive gastric acid and pancreatic amylase secretion were determined in 10 young smokers (mean age 23 years) and 7 nonsmokers (mean age 26 years). There was no significant difference in the length of the interdigestive motor complex between smokers and nonsmokers, but the speed of transmission of the activity front (phase III) in the upper intestine was significantly (p less than 0.05) greater in smokers than in nonsmokers. No significant overall changes in the interdigestive gastric acid and pancreatic amylase outputs were observed between the two groups studied.

Abnormalities in gastrointestinal motor activity in patients with short bowels: Effect of a synthetic opiate

We have investigated the fasting and postprandial patterns of gastrointestinal pressure activity in a group of patients with extensive (>100 cm) resections of the distal small bowel. Each short bowel patient was studied on 2 consecutive days with random single blind administration of either loperamide (6 mg at 5 h and at 30 min before the meal) or placebo, and 20 healthy controls were studied on single days (13 basal fasting, 7 placebo). During fasting, the duration of the interdigestive motor complex was significantly shorter in patients with short bowel syndrome (71.1 ± 15.6 min vs. 109 ± 7.8 min for controls, p < 0.03); hence, the frequency of complexes was increased. The duration of phase 2 was strikingly shorter in patients (18.7 ± 7.0 min vs. 52.9 ± 8.5 min for controls, p < 0.03). Gastric emptying and postprandial motor activity were identical in patients and controls. During fasting, loperamide prolonged phase 3 (7.6 ± 2.2 min vs. 4.3 ± 1.1 min for placebo, p < 0.03). Postprandially, loperamide shortened the time from meal ingestion to the first phase 3 by 50% (p < 0.003), and increased motility index and frequency of contraction in the gut (p < 0.01). Thus, gut motor activity in the short bowel syndrome is characterized by more frequent interdigestive motor complexes, marked reduction in phase 2 activity, and a normal feeding pattern. Loperamide therapy increases feeding activity while at the same time shortening its duration.

Interdigestive motilin secretion and gallstone disease.

Plasma motilin concentrations were measured in eight controls and 11 patients with radiolucent gallstones over a period of 3-4 h following an overnight fast. In five of these patients the interdigestive motor complex (IDMC) was studied simultaneously. The results indicate: a) cyclical changes of plasma motilin concentrations (mean cycle duration 110 +/- 9.9 and 102 +/- 8.4 min, means +/- SEM) and a significant correlation between the basal intercyclical motilin concentrations and the age (p less than 0.02) in the controls and the gallstone patients studied, and b) a significant correlation between the maximal motilin increase and the age in the controls (p less than 0.01) but not in the gallstone patients. The results therefore suggest a different behaviour of the interdigestive motilin patterns in controls and gallstone patients. As the motilin cycles were accompanied in 90% with an IDMC in the five patients studied this conclusion might include an abnormal interdigestive motor activity within the intestinal tract in gallstone patients.

Interdigestive phasic contractions of the human lower esophageal sphincter

The results of this study show that lower esophageal sphincter contractions occur during phases 2 and 3 of the gastric interdigestive migratory motor complex in humans. In one series of studies, esophageal, gastric, and duodenal pressures were monitored overnight for 12 h in 7 healthy, fasting subjects. A second group of 10 volunteers was studied for 12 h on two consecutive nights. Periods of gastric contraction that reached a maximum frequency of about 3/min were shown to be part of the migratory motor complex cycle because they occurred immediately before phase 3 migratory motor complex activity in the duodenum. In all subjects, gastric interdigestive contractions were accompanied by lower esophageal sphincter contractions that maintained a pressure barrier between the stomach and esophageal body. During Jate phase 2 and phase 3 gastric migratory motor complex activity, the lower esophageal sphincter contractions were especially vigorous. Mean basal lower esophageal sphincter pressure varied significantly during the interdigestive cycle. Lower esophageal sphincter pressure values were maximal during phase 3 of gastric migratory motor complex activity and minimal values occurred during phase 1. No episodes of gastroesphageal reflux occurred as a result of increase of intragastric pressure caused by interdigestive gastric contractions. The coupling of lower esophageal sphincter contractions to interdigestive gastric contractions appears to be an important physiological mechanism for preventing gastroesophageal reflux during forceful gastric contractions.