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PubMed1987

The effect of insulin-induced hypoglycaemia on gastrointestinal motility in man.

The effect of insulin-induced hypoglycaemia on gastro-jejunal motility was studied in five, healthy, male subjects using tethered, pressure sensitive, radiotelemetry capsules. Thirty minutes after the intravenous injection of soluble insulin (0.15 unit/kg body weight), a significant reduction in blood glucose concentration (control: 5.26 +/- 0.19 SEM mmol/l; insulin: 1.48 +/- 0.44 mmol/l; P less than 0.001) was associated with a rise in heart rate (mean peak rise 29 +/- 8 beats/min, P less than 0.05), systolic arterial blood pressure (mean peak rise 28 +/- 4 mmHg, P less than 0.01) and plasma pancreatic polypeptide concentration (control: 20 +/- 7 pmol/l; insulin: 287 +/- 66 pmol/l; P less than 0.01). These events coincided with a short period of jejunal motor activity, which was not associated with gastric motor activity nor with raised plasma motilin concentrations. During the control study, there were no changes in blood glucose concentration, heart rate, arterial blood pressure or plasma pancreatic polypeptide concentrations, and there was no jejunal motor activity. The interval between successive gastric migrating motor complexes (MMC) was not significantly different in the insulin and control studies (control: median interval 110 min, range 108-148 min; insulin: median interval 124 min, range 115-125 min), suggesting that the fasting gastrojejunal MMC and jejunal motor activity arose independently. Insulin-induced hypoglycaemia is accompanied by jejunal motor activity, which may underlie the abdominal symptoms associated with hypoglycaemia.

Adult↗
PubMed2004

Review article: serotonin receptors and transporters -- roles in normal and abnormal gastrointestinal motility.

The gut is the only organ that can display reflexes and integrative neuronal activity even when isolated from the central nervous system. This activity can be triggered by luminal stimuli that are detected by nerves via epithelial intermediation. Epithelial enterochromaffin cells act as sensory transducers that activate the mucosal processes of both intrinsic and extrinsic primary afferent neurones through their release of 5-hydroxytryptamine (5-HT). Intrinsic primary afferent neurones are present in both the submucosal and myenteric plexuses. Peristaltic and secretory reflexes are initiated by submucosal intrinsic primary afferent neurones, which are stimulated by 5-HT acting at 5-HT(1P) receptors. 5-HT acting at 5-HT4 receptors enhances the release of transmitters from their terminals and from other terminals in prokinetic reflex pathways. Signalling to the central nervous system is predominantly 5-HT3 mediated, although serotonergic transmission within the enteric nervous system and the activation of myenteric intrinsic primary afferent neurones are also 5-HT3 mediated. The differential distribution of 5-HT receptor subtypes makes it possible to use 5-HT3 antagonists and 5-HT4 agonists to treat intestinal discomfort and motility. 5-HT3 antagonists alleviate the nausea and vomiting associated with cancer chemotherapy and the discomfort from the bowel in irritable bowel syndrome; however, because 5-HT-mediated fast neurotransmission within the enteric nervous system and the stimulation of mucosal processes of myenteric intrinsic primary afferent neurones are 5-HT3 mediated, 5-HT3 antagonists tend to be constipating and should be used only when pre-existing constipation is not a significant component of the problem to be treated. In contrast, 5-HT4 agonists, such as tegaserod, are safe and effective in the treatment of irritable bowel syndrome with constipation and chronic constipation. They do not stimulate nociceptive extrinsic nerves nor initiate peristaltic and secretory reflexes. Instead, they rely on natural stimuli to activate reflexes, which they strengthen by enhancing the release of transmitters in prokinetic pathways. Finally, when all the signalling by 5-HT is over, its action is terminated by uptake into enterocytes or neurones, which is mediated by the serotonin reuptake transporter. In inflammation, serotonergic signalling is specifically diminished in the mucosa. Transcripts encoding tryptophan hydroxylase-1 and serotonin reuptake transporter are both markedly decreased. Successive potentiation of 5-HT and/or desensitization of its receptor could account for the symptoms seen in diarrhoea-predominant and constipation-predominant irritable bowel syndrome, respectively. Symptoms associated with the down-regulation of the serotonin reuptake transporter in the human mucosa in irritable bowel syndrome are similar to the symptoms associated with the knockout of the serotonin reuptake transporter in mice. The observation that molecular defects occur in the human gut in irritable bowel syndrome strengthens the hand of those seeking to legitimize the disease. At least it is not 'all in your head'. The bowel contributes.

Central Nervous System↗
PubMed1996

Coordination of biliary and upper gastrointestinal motility in the fasted conscious pig.

A chronic pig model was developed which permits the simultaneous measurement of integrated biliary motility as resistance to flow (CBD inflow), gallbladder, duodenal and gastric motility in addition to collection of venous blood samples for gut hormones estimations. Animals displayed a duodenal interdigestive cycle of 55.4 +/- 3.4 min (mean +/- SEM, n = 6), consisting of phase I, II and III (21.2 +/- 2.1, 70.5 +/- 2.0, 8.7 +/- 0.5% of the cycle, respectively). A gastric interdigestive cycle of 60.2 +/- 6.5 min (n = 4) was similarly demonstrated consisting of three phases which corresponded to the three duodenal phases. The gastric phases I, II and III comprised 26.3 +/- 3.0, 71.2 +/- 2.7 and 2.5 +/- 0.8% of the cycle, respectively. The gastric phase III immediately preceded the onset of the duodenal phase III. The gallbladder likewise displayed an interdigestive cycle of 54.5 +/- 7.2 min (n = 6) consisting of a quiescent period (37.2 +/- 3.7% of the cycle) corresponding temporally to duodenal phase III and phase I. This quiescent phase was followed by a period of rhythmic contractions (64.5 +/- 4.1% of the cycle) which corresponded temporally to duodenal phase II. The onset of the gallbladder quiescent period coincided with the onset of duodenal phase III. The CBD inflow similarly demonstrated an interdigestive cycle of 53.4 +/- 9.6 min (n = 4) duration, consisting of three phases. The initial phase was evident as a period of rapid inflow, the onset of which coincided with the onset of duodenal phase III and the gallbladder quiescent period, and occupied 12.0 +/- 0.8% of the cycle. The second phase which occupied 18.0 +/- 7.4% of the cycle, was typified as a period of declining inflow which reached a relatively stable level at a time corresponding to the end of duodenal phase I. The third phase consisted of the maintenance of the inflow rate achieved at the end of the previous phase (60% of maximum inflow), corresponding in onset and duration with duodenal phase II and occupied 70.0 +/- 8.6% of the cycle. Plasma motilin levels fluctuated in relation to the duodenal interdigestive cycle, peaking during phase III relative to phase I (36.9 +/- 8.5 vs 25.4 +/- 7.7 pg mL-1, respectively, n = 5, P < 0.05). Cholecystokinin levels did not fluctuate, remaining low (2.3 +/- 2.1 pM cholecystokinin octapeptide equivalents, n = 5) throughout the duodenal interdigestive cycle, but increased about two fold after ingestion of solid food. Feeding disrupted the gastric, duodenal, gallbladder and CBD inflow cycles.

Animals↗
PubMed2004

Tracking the moveable feast: sonomicrometry and gastrointestinal motility.

Ultrasonomicrometry measures distance between piezoelectric crystals based on transmission time of ultrasound bursts. It allows monitoring of coordinated motion of small and delicate tissues, including gastrointestinal sphincters. Its suitability for motility studies in small animals such as mice suggests that its use in gastrointestinal studies will increase in coming years.

Animals↗
PubMed1992

Review article: 5-hydroxytryptamine agonists and antagonists in the modulation of gastrointestinal motility and sensation: clinical implications.

Serotonin (5-hydroxytryptamine; 5-HT) is found in the enteric nervous system where it has been implicated in controlling gastrointestinal motor function. A number of receptor or recognition sites have been identified in the gut, but recently most attention has focused on the 5-HT3 and 5-HT4 receptors. The functional role of the 5-HT3 receptor remains incompletely understood, but it is probably involved in the modulation of colonic motility and visceral pain in the gut. A number of selective 5-HT3 antagonists have been developed including ondansetron, granisetron, tropisetron renzapride and zacopride. While the substituted benzamide prokinetics (for example, metoclopramide, cisapride) also block 5-HT3 receptors in high concentrations, their prokinetic action is believed to be on the basis of their agonist effects on the putative 5-HT4 receptor. Some 5-HT3 antagonists have 5-HT4 agonist activity (for example, renzapride, zacopride) and others do not (for example, ondansetron, granisetron), while tropisetron in high concentrations is a 5-HT4 antagonist. Based on the pharmacological data, it has been suggested that specific 5-HT antagonists and agonists may prove to be beneficial in a number of gastrointestinal disorders including the irritable bowel syndrome, functional dyspepsia, non-cardiac chest pain, gastrooesophageal reflux and refractory nausea. In this review, the rationale for the use of these compounds is discussed, and the available experimental evidence is summarized.

Carcinoid Tumor↗
PubMed2000

Effects of very long chain versus long chain triglycerides on gastrointestinal motility and hormone release in humans.

Fish oil (a very long chain triglycerides, VLCT) has received much attention because of its favorable metabolic properties; however, its effect on gastrointestinal function has not been studied. We investigated the effects of intraduodenally administered VLCT on gut-hormone release [cholecystokinin (CCK), neurotensin, peptide YY (PYY)], gallbladder emptying, antroduodenal motility, and small bowel transit time (SBTT) in comparison to intraduodenal administration of saline and long chain triglycerides (LCT, corn oil) in nine healthy volunteers. Gallbladder contraction duration was significantly shorter after VLCT than after LCT (138 +/- 16 min vs 233 +/- 38 min, P < 0.05). Both fats induced a fed motility pattern, while SBTT was not significantly altered. CCK secretion was significantly reduced after VLCT compared to LCT (36 +/- 12 pM x 120 min vs 78 +/- 15 pM x 120 min, P < 0.05), whereas PYY and neurotensin release were not significantly different. In conclusion, effects of triglycerides on CCK and gallbladder motility appear to be chain-length dependent, in contrast to the effects on distal gut-hormone release and intestinal motility and transit, which appear to be chain-length independent.

Adolescent↗
PubMed1991

[Influence of the ileum on the regulation of gastrointestinal motility].

Under normal conditions a "physiologic malabsorption" and thus nutrients in the lower small intestine in the late postprandial state can be observed in humans. To study the effects of "physiologic" quantities of nutrients in the distal small intestine on upper gastrointestinal motor functions, 9 healthy subjects were intubated with an oro-ileal multi-lumen tube. The continuous perfusion of the duodenum with essential amino acids induced a fed motility pattern. In 12 out of 14 cases additional ileal perfusion with carbohydrates (60 kcal), but not with saline, converted the fed motility pattern to a pattern characteristic of the interdigestive state. These findings suggest that the ileum takes part in the late postprandial regulation of proximal gastrointestinal motor functions in humans.

Amino Acids, Essential↗
PubMed2003

Effect of peppermint oil and caraway oil on gastrointestinal motility in healthy volunteers: a pharmacodynamic study using simultaneous determination of gastric and gall-bladder emptying and orocaecal transit time.

BACKGROUND: Although peppermint oil and caraway oil are frequently used in herbal drugs for abdominal discomfort and pain, the pharmacological insights into their effects on the gastrointestinal tract are poor. METHODS: The pharmacodynamic effects of 90 mg peppermint oil (WS 1340) and 50 mg caraway oil (WS 1520) on the motility of the stomach and gall-bladder, and on the orocaecal transit time, in comparison with placebo, 10 mg cisapride and 10 mg n-butylscopolamine, were studied in 12 healthy volunteers. The study involved simultaneous ultrasonic determination of gastric and gall-bladder emptying, together with assessment of the orocaecal transit time using the lactulose H2 breath test. The combination of these methods allows three gastrointestinal organs to be studied in one subject simultaneously. RESULTS: The antral filling time was comparable with placebo, peppermint oil, caraway oil and cisapride, whereas it was significantly shortened (P = 0.04, two-sided paired t-test) with n-butylscopolamine. The gastric emptying time did not differ significantly between placebo, peppermint oil, caraway oil and cisapride, but was significantly prolonged by n-butylscopolamine (P = 0.04, two-sided paired t-test). Complete inhibition of gall-bladder emptying was caused by both oils and n-butylscopolamine. Cisapride significantly shortened gall-bladder emptying compared with placebo (P = 0.02, two-sided signed rank test). The orocaecal transit time was significantly prolonged by peppermint oil (P = 0.004) and n-butylscopolamine (P = 0.002), but not significantly prolonged by caraway oil (P = 0.06); it was significantly shortened by cisapride (P = 0.04, all two-sided paired t-test). CONCLUSIONS: Peppermint oil and caraway oil show a relaxing effect on the gall-bladder and the former slows small intestinal transit. Further studies should investigate the effects of both oils on a maximal contraction stimulus on the gall-bladder, and in patients suffering from motility disorders.

Adult↗
PubMed1999

Control systems of gastrointestinal motility are immature at birth in dogs.

Networks of interstitial cells of Cajal (ICC) in the myenteric plexus (Myp) or circular muscle (CM) function as pacemakers for gastrointestinal slow waves. ICC in contact with muscle and closely associated with nerves in the CM may mediate inhibitory neurotransmission. We wondered if ICC in Myp and CM and their connections are immature at birth and mature first in the proximal gut in association with nerves. Tissues from lower esophageal sphincter (LES), pylorus (PYL), small intestine (SI) and colon (CO) of 18 term fetal dogs taken from six females were fixed and prepared for ultrastructural examination and studied. Ganglia were present where expected in the Myp and submucous plexus (SMP). ICC cells were present in the Myp of PYL, SI and CO and appeared to have normal relationships to the outer border of CM as in adults. ICC in CM were found associated with nerves in the LES and in PYL, but not in SI or CO. However, axons in CM were everywhere usually free of glial covering, indicating ongoing migration or development. No organized deep muscular plexus (DMP) in SI or submuscular plexus (SP) in colon was present. Visible gap junctions were absent everywhere except for very rare ones between circular muscle cells. We conclude that at birth the neural and ICC networks of CM are more immature in intestine and colon than in oesophagus and stomach. Development of nerve and ICC of CM in oesophagus and stomach apparently precedes that in the remaining gut. However networks in these regions have not achieved adult organization and ICC and smooth muscle cells are anatomically poorly coupled. These findings suggest the reasons that gut motility at birth will not be adult in pattern are because ICC, nerve and muscle control systems are not fully differentiated. Further developmental delays in ICC and nerve maturation could have serious consequences for feeding of infant animals.

Animals↗
PubMed1991

Abnormalities of gastrointestinal motility in children with nonulcer dyspepsia and in children with gastroesophageal reflux disease.

In 11 children (mean age 44.2 months) with symptoms suggesting upper intestinal dysfunction (nonulcer dyspepsia), in nine children (mean age 27.3 months) with gastroesophageal reflux (GER) disease, and in seven controls (mean age 20.4 months) we investigated fasting [for 3 hr or until two migrating motor complexes (MMC) were observed] and fed (90 min) antroduodenal motility by means of perfused catheter system; furthermore, we measured both gastric emptying of a radiolabeled milk formula and fasting duodenogastric reflux during manometry by assessing bile salt concentration in gastric aspirates. No structural abnormalities of gastrointestinal tract and organic disorders were detected in the patients. In a high proportion of both groups of patients we found manometric abnormalities of interdigestive and fed motor patterns that were not seen in the controls: absence of antral phase III of MMC; significant decrease of antral and/or duodenal motor activity during fasting and/or fed periods; abnormal propagation or configuration of MMC phase III that was significantly shorter than in controls; bursts of sustained fasting and/or fed phasic duodenal activity, frequently uncoordinated with adjacent gut segments. When compared to controls, the mean intragastric concentration of bile salts during all MMC phases and the mean 1-hr percent gastric activity of the radiolabeled milk were significantly higher in the two groups of patients. We conclude that in a high proportion of children with nonulcer dyspepsia and of children with GER disease, gastrointestinal manometry may reveal significant irregularities of antral and duodenal motility, which are associated with increased duodenogastric reflux and delayed gastric emptying.

Bile Acids and Salts↗
PubMed1990

Disorders of gastrointestinal motility in neurologic diseases.

Neurologic diseases can affect the bowel at several levels of innervation--by altering the electrical activity that controls smooth muscle, the enteric nervous system, or the extrinsic neural pathways to the gut. This review concentrates on disorders of motility that occur in conjunction with diseases of the extrinsic neural supply (from the level of the brain to the postganglionic fibers) and those generalized disorders that affect gut smooth muscle. Modern technology, such as gastrointestinal scintigraphy and manometric techniques that measure esophageal, gastroduodenal, and anorectal motility (intraluminal pressures), has provided better methods to study the pathophysiologic aspects of gut motility in diseases of the nervous system. Distinguishing the neuropathies of the extrinsic nervous system from those of the intrinsic (enteric) nervous system is not always possible because the available techniques evaluate only the end-organ--that is, the motor function of the gut. Degenerative or infiltrative (myopathic) disorders of gut smooth muscle, however, can be distinguished from such neuropathies, and careful and systematic evaluation of autonomic function can often identify the level of disordered function in the neural-gut axis.

Autonomic Nervous System Diseases↗
PubMed2004

[Gastrointestinal motility disturbances in Chagas disease].

UNLABELLED: Serum antibodies against Trypanosoma Cruzi have been observed in 19% of the Chilean population. Marked differences in organ involvement have been reported in patients with Chagas disease. Chagas disease is rarely an aetiological factor for achalasia in Chile, which is different from reports in other countries of South America. In contrast, a high incidence of megacolon among these patients have been reported. AIM: To study the incidence of gastric and small intestinal motor disorders among these patients and their relationship to esophageal and colon motility disorders. PATIENTS AND METHODS: We studied 18 patients, 12 women (mean age 45 years); with positive antibodies against T. Cruzi. Seven had radiological evidence of megacolon and no one had radiological or manometric evidence for achalasia. Non specific motor esophageal abnormalities were found in 11 patients. Nine had an abnormal electrocardiogram, suggesting a myocardial disease. A questionnaire for gastrointestinal symptoms, an electrogastrography and a small intestinal motility study, were performed in each patient. RESULTS: All patients had evidences of abnormalities in at least one segment of the digestive tract. Twelve patients had an abnormal electrogastrographic study, with bradygastria as the most common finding. Nine had an abnormal small intestinal manometry with a myophatic pattern evidenced by a decreased amplitude of contractions (18.5 +/- 3 mmHg). Also an increased number of clustered contractions was observed. CONCLUSIONS: Gastric dysrhythmias and small intestinal motor abnormalities are frequently associated to non specific esophageal motor disorders and megacolon in patients with Chagas disease.

Adolescent↗
PubMedDate not supplied

Gastrointestinal motility of patients with Roux-en-Y reconstruction.

The electromyographic activity of the gastrointestinal tract was studied in 28 patients undergoing gastric, biliary, and pancreatic operations with reconstruction of the gastrointestinal tract with a Roux-en-Y limb. The Roux-en-Y limb was constructed 1 to 5 years before the study in 8 patients (chronic Roux-en-Y) and at the operation in which the electrodes were implanted in 20 patients (recent Roux-en-Y). All four phases of the migrating motor complex (MMC) were identified in the gastrointestinal tract, including in the Roux-en-Y limb. The duration of the MMC was 82.4 +/- 22.3 min in the patients with chronic Roux-en-Y and 89.0 +/- 25.1 min in the patients with recent Roux-en-Y. Food ingestion converted the MMC to the fed pattern in the entire gastrointestinal tract, including the Roux-en-Y limb in 16 (76.2%) of 21 recordings of the patients with chronic Roux-en-Y and in 27 (84.4%) of 32 recordings of the patients with recent Roux-en-Y. The duration of the fed pattern was 170 +/- 34 min in the patients with chronic Roux-en-Y and 154 +/- 26 min in the patients with recent Roux-en-Y. The findings of this study indicate that the electromyographic activity of the Roux-en-Y limb is normal during both fasting and fed states, even many years after the construction of the Roux-en-Y.

Anastomosis, Roux-en-Y↗
PubMed1986

Dose-related effects of synthetic human beta-endorphin and naloxone on fed gastrointestinal motility.

In humans, plasma beta-endorphin levels rise during application of acute stressful stimuli (vertigo, cold pain, and transcutaneous electrical stimulation) that induce gut motor disturbances. Whereas it is possible that circulating beta-endorphin participates in the mediation of these central effects on gut motility, its role cannot be established solely on the basis of changes in plasma levels. Therefore, we designed the present study to investigate 1) the dose-related effects of intravenous synthetic human beta-endorphin and naloxone on gastrointestinal pressure activity in fed healthy individuals; and 2) the interactions of the opiate agonist and antagonist. Infusion of beta-endorphin increased pyloric phasic pressure activity (P less than 0.001) and induced intestinal bursts of rhythmic activity (P less than 0.05) which interrupted normal fed motility. These effects were dose related, with the pyloric dose-response profile being essentially linear. The effects in the proximal intestine were obtained with doses of beta-endorphin at 250 ng X kg-1 X min-1 or greater. In the antrum, there was an overall reduction in phasic pressure activity (P less than 0.02), which was predominantly an effect of the highest dose of beta-endorphin infused (2,500 ng X kg-1 X min-1). Naloxone by itself had no significant effect on fed upper gut motility. However, naloxone significantly inhibited the effect of the lower doses of beta-endorphin on the pylorus. In addition, naloxone significantly reduced the probability of beta-endorphin, triggering intestinal bursts of rhythmic activity. These data suggest that beta-endorphin may play a humoral role in the stimulation of fed pyloric contraction at physiological levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Does disordered upper gastrointestinal motility predispose to Helicobacter pylori colonization of the stomach in children?

Helicobacter pylori is an important factor in the pathogenesis of chronic gastritis and gastroduodenal ulcer disease. However, the basic causal mechanisms of H pylori colonization on the gastric mucosa are still unclear. The authors evaluated the prevalence of H pylori colonization in 266 children who underwent upper gastrointestinal endoscopy during a 12-month period. The indications for endoscopy were follow-up of esophagitis related to gastroesophageal reflux (n = 17), suspicion of gastroesophageal reflux (n = 51), abdominal pain (n = 28), vomiting (n = 30), follow-up of esophageal atresia (n = 46) and duodenal atresia (n = 28), inflammatory bowel disease (n = 28), and miscellaneous (n = 38). The methods used to detect H pylori colonization were histology and the rapid urease test. H pylori colonization was demonstrated in 31 (11.6%) of the 266 patients. In two patient groups, a high prevalence of colonization was identified. In patients with an operated duodenal atresia, 36% (10 of 28) had H pylori on the gastric mucosa. The organism was demonstrated on the gastric mucosa in 47% (8 of 17) of the patients with gastroesophageal reflux-related esophagitis; five of the eight patients had neurological impairment. In the other patient groups, the prevalence of H pylori infection ranged from 2% to 14%. The present study suggests that, in children, the disturbed esophagogastroduodenal motility, which is commonly associated with gastroesophageal reflux and duodenal atresia, predisposes to H pylori infection.

Adolescent↗
PubMed1982

Drugs increasing gastrointestinal motility.

Studies in animals and man have shown that metoclopramide, bethanechol and domperidone enhance the peristaltic contractions of the esophageal body, increase the muscle tone of the lower esophageal sphincter, and stimulate gastric motor activity. The drugs have been found to be beneficial in the treatment of gastric motor failure and of reflux esophagitis secondary to lower esophageal sphincter incompetence. Metoclopramide and domperidone, unlike bethanechol, do not increase gastric acid secretion. Whilst bethanechol directly stimulates the muscarine receptors of gastrointestinal smooth muscle, metoclopramide is assumed to act indirectly, i.e. through an increase in acetylcholine release. Domperidone antagonizes noradrenaline- and dopamine-induced relaxations of guinea pig isolated smooth muscle preparations. Since there is no evidence for the occurrence of specific dopamine receptors in the esophagus, stomach or ileum of guinea pigs, domperidone is supposed to affect motility, at least in this species, through blockade of alpha 1-adrenoceptors.

Animals↗