Effects of ileal bile salts on fasting small intestinal and gallbladder motility

In the fasting state, gallbladder emptying is related to phase III of the intestinal migrating motor complex. The effects of ileal infusion of mixed taurocholate-phospholipid micelles on fasting small intestinal motility (by a 17-channel catheter with side holes located in duodenum, jejunum and ileum) and gallbladder motility (by ultrasound) were investigated in eight healthy volunteers. After bile salt depletion by cholestyramine, 0.9% NaCl or mixed micelles were infused in the ileum during phase II of the migrating motor complex. Time to onset of subsequent phase III was significantly shorter after infusion of mixed micelles compared with 0.9% NaCl (32 +/- 5 min vs. 60 +/- 5 min, P = 0.01). Distal to the infusion port, numbers of pressure waves and their amplitudes were significantly lower during bile salt infusion compared with 15 min before infusion (11 +/- 6 per 15 min vs. 21 +/- 8 per 15 min, and 2.4 +/- 0.6 kPa vs. 2.8 +/- 0.5 kPa, respectively). Micellar infusions increased fasting gallbladder volumes to 170 +/- 5% of starting volumes (P < 0.0001). In conclusion, ileal infusion of mixed micelles influences the timing of phase III of the intestinal migrating motor complex, inhibits ileal motility and increases fasting gallbladder volumes. These findings may have important consequences for enterohepatic circulation of bile salts.     

Plasma Motilin Variation During the Interdigestive and Digestive States in Man

To evaluate the role of motilin in human physiology, we measured plasma motilin during the inter digestive and digestive states while recording antroduodenal contractile activity. In 24 healthy fasting subjects, 51 migrating periods of phase III activity were recognized, 42 of them started from the antral region and nine from the duodenum. A definite association was noted between circulating motilin and the gastric migrating motor complex. Significant peak elevations in plasma motilin were associated with phase Ills initiated from the antrum, but not with those originating from the duodenum. Exogenous synthetic motilin, when administered in supraphysiologic amounts, induced premature periods of front activity in fasting subjects. A test meal administered 30 minutes after a front of antral activity induced a significant release of motilin. Elevated plasma motilin levels were detected postprandially for a period of 30 minutes. Postprandial motilin increases were comparable in amplitude to the cyclic peak increases observed during the fasting period. Our study brings support for the argument that the contractile activity of the fasting stomach is regulated by circulating motilin in man, as it is in animals. The documented postprandial release of motilin is, however, unique to man and suggests that motilin could also be active during the digestive period in this species.     

Post-prandial and interdigestive return of bile acids to the gallbladder in healthy subjects

The enterohepatic circulation of a radioactive marked bile acid (⁷⁵Se-HCAT) was studied by scintigraphy in the post-prandial period as well as after prolonged fasting in healthy young male volunteers in combination with a continuous pressure recording from the antroduodenal region. In a group of 8 subjects the radioactive marker was instilled into duodenum after the ingestion of a standard meal. At the transition from fed-motility pattern (irregular contractions with a frequency of 1–9 per minute) to fasting intestinal motility pattern, defined as the occurrence of a Phase HI activity-front of the migrating motor complexes, a median (range) of 14% (9–25%) of the ⁷⁵Se-HCAT pool was stored in the gallbladder. During the following migrating motor complex cycles, net gallbladder filling occurred with a significantly higher rate during Phase I (0.22% of the ⁷⁵Se-HCAT pool per minute) compared to Phase II, where the median net value was 0.07%. This difference in net filling rate was due to the occurrence of periods of gallbladder emptyings during Phase II. At the end of this first migrating motor complex cycle in the post-prandial period a total of 32% (26–46%) of the ⁷⁵Se-HCAT pool was in the gallbladder. In another group of 8 subjects the scintigraphic study was not carried out until 15–20 hours after ingestion of the standard meal and the radioactive marker. The scintigraphic study was carried out for two subsequent migrating motor complex cycles, and the amount of the ⁷⁵Se-HCAT pool present in the gallbladder at the first recorded Phase III complex was 46% (32–52%). The figures at the occurrence of the following two Phase III complexes were 48% (32–65%) and 47% (42–59%), respectively. A cyclic variation in gallbladder filling and emptying in connection with the migrating motor complex cycle was seen with a net filling during Phase I and a net emptying during Phase II. In the study after prolonged fasting the number and duration of the spontaneous gallbladder emptyings in Phase II were not different from those in the post-prandial study. However, the amount emptied in per cent of the ⁷⁵Se-HCAT pool was significantly higher in the group studied after prolonged fasting compared to the group studied in the postprandial period, and accounted for a median of 3.3% (2.0–16.5%) and (1.6–6.0%) of the ⁷⁵Se-HCAT pool, respectively. This difference is most likely due to an increase in the concentration of gallbladder bile during fasting.     

Effects of motilin on human interdigestive gastrointestinal and gallbladder motility, and involvement of 5HT3 receptors.

A plasma motilin peak and a partial gallbladder emptying precede the antral phase III of the migrating motor complex (MMC). To clarify the causal relationship between these factors, we aimed to study the role of motilin in interdigestive gastrointestinal and gallbladder motility simultaneously. In addition, involvement of 5HT3 receptors in the action of motilin was studied. Eight fasting, healthy male volunteers received 13Leu-motilin or 0.9% NaCl i.v. for 30 min, in randomized order on two separate occasions, from 30 min after phase III. Seven of the eight subjects also received the 5HT3 receptor antagonist ondansetron in addition to motilin, on a third occasion. Antroduodenal motility, gallbladder volumes and plasma motilin were measured. The interval between the start of infusion and phase III was 95.0 (57.6-155.7) min for saline, 28.7 (21.0-33.2) min for motilin, and 39.3 (30.7-100.5) min for motilin + ondansetron (P < 0.05). Gallbladder volume decreased by one-third from 10 min after both motilin and motilin + ondansetron infusion (P < 0.05), and returned to baseline with duodenal passage of phase III. In two of the seven subjects phase III was absent after motilin + ondansetron, although gallbladder volume decreased and only refilled during a later spontaneous phase III. We conclude that motilin induces both partial gallbladder emptying and antral phase III. Indeed, although gallbladder emptying clearly precedes antral phase III, ondansetron only prevented phase III in some cases and had no effect on gallbladder emptying. Passage of phase III in the duodenum makes an important contribution to gallbladder refilling.     

49Sibutramine accelerates gastric emptying, inhibits intestinal motility in conscious dogs

Fasting interdigestive myoelectric complex (IMC) and postprandial gastroduodenal myoelectric activities are regulated by motilin and leptin, respectively (L. Zhou 2005). This study is to observe whether electrical acupuncture points could increase fasting gastroduodenal IMC and postprandial activities, as well as increase the release of motilin and leptin. Methods: Bipolar platinum electrodes were implanted on the serosa of antrum and duodenum in 10 conscious Wistar rats to record IMC and postprandial digestive myoelectric activities. We acupunctured Points Zusanli (S‐36), Tianshu (S‐25), and Liangmen (S‐21) during phase I of IMC (Frequency 20~100 Hz, Strengthen 12~16 mA, period 90 min) and compared with non‐specific electric stimulation (sham acupuncture) group. Serum motilin and leptin level was measured by RIA. Results: (1) Acupuncture points could shorten markedly phase I of antroduodenal IMC and increase the period of phase III (P < 0.01). Acupuncture points also increased the number of spike burst of antral and duodenal slow wave by (121.24 ± 20.0)% and (97.34 ± 15.20)% (compared with control group, P < 0.01). In postprandial period, acupuncture points could increase the number of spike burst of antral and duodenal slow wave by (142.52 ± 23.50)% and (102.48 ± 13.25)% (compared with control group, P < 0.01). (2) When acupuncture points increased the number of spike burst of IMC in fasting state, serum motilin concentration also increased, which was (74.56 ± 8.20)% more than control group (P < 0.01). When acupuncture points with meal, serum leptin concentration increased with myoelectric activity, which was (139.84 ± 20.25)% more than control group (P < 0.01). There was no change of motilin and leptin concentration in non‐specific electric stimulation group. (3) Cutting off subphrenic vagus nerves could totally block the effect of acupuncture points on antroduodenal myoelectric activities and release of motilin and leptin. Conclusions: Acupuncture points could effectively increase fasting and postprandial antroduodenal myoelectric activities. This effect is mediated by motilin and leptin, respectively.     

μ-Opiate receptor agonist loperamide blocks bethanechol-induced gallbladder contraction, despite higher cholecystokinin plasma levels in man

mu-Opiate receptor agonists, such as loperamide, influence biliary excretion and suppress cholecystokinin (CCK)-induced gallbladder contraction. Loperamide decreases cholinergic mechanisms, like pancreatic polypeptide (PP) release, while muscarinic agonist (bethanechol)-induced PP release remains unaffected. The effects of loperamide on gallbladder contraction and peptide release were performed to resolve this discrepancy. METHODS: Six subjects (27.6 +/- 2.0 years) received bethanechol (12.5, 25 and 50 microg kg(-1) h(-1) continuously over 40 min) after oral 16 mg loperamide (vs placebo) in a crossover design. Gallbladder volume and plasma levels of CCK, PP, motilin, gastrin, neurotensin, cholylglycine were measured regularly. RESULTS: Bethanechol significantly reduced gallbladder volume (26.7 +/- 1.9 to a nadir of 15.3 +/- 2.2 mL, P < or = 0.05), and this action was inhibited by loperamide. Basal CCK levels increased significantly after loperamide. Incremental integrated CCK release after bethanechol was higher under loperamide (P < or = 0.05), as placebo CCK release was significantly decreased under bethanechol (2.0 +/- 0.4-0.8 +/- 0.3 pmol L(-1)). In both settings, PP levels were significantly increased after bethanechol, while release of neurotensin, motilin, gastrin and cholylglycine was unaffected. CONCLUSION: The mu-opiate receptor agonist loperamide inhibits bethanechol-induced gallbladder contraction. This effect is not mediated by inhibition of CCK release, as loperamide even enhances basal CCK plasma levels. As cholinergic mechanisms, like bethanechol-induced incremental PP release, were unaffected, mu-opiate agonists might influence gallbladder contraction via vagal-cholinergic pathways.     

Role of Cholecystokinin in Gallbladder and Duodenal Motility in the Interdigestive State of Dogs

This study was designed to determine the role of cholecystokinin (CCK) in the motility patterns of duodenum and gallbladder in fasted conscious dogs. During the naturally occurring activity front in the duodenum a significant increase in the motility index, (MI) of the gallbladder was accompanied by a decrease in the gallbladder volume from about 28 ± 4 ml (control) to 21 ± 3 ml. Similar changes in the gallbladder were observed after intravenous bolus injections of motilin (20 to 40 ng/kg), which gave increments in plasma motilin comparable to those occurring spontaneously during the activity front but failed to affect plasma levels of CCK. Blocking of CCK receptors by L-364, 718 (0.5 to 1 mg/kg) delayed the occurrence of the spontaneous activity front in the duodenum and the accompanying alterations in the gallbladder motility. CCK receptor antagonism abolished the premature activity front induced by motilin in both the duodenum and the gallbladder, converted the fed-like pattern induced by exogenous CCK to a fasted motility pattern in the duodenum and prevented CCK-induced reduction in the gallbladder volume. Atropine (12.5 μg/kg) blocked the spontaneous activity front in the duodenum and accompanying alterations in the gallbladder motility and volume but failed to affect those induced by motilin. We conclude that the motility of the gallbladder in fasted dogs shows cyclic changes with typical reduction in the organ volume coinciding with the spontaneous or motilin-induced activity front in the duodenum, and that both CCK and muscarinic receptors are involved in the MMC-related alterations in the motor activity of the gallbladder.     

Phase III of the migrating motor complex: associated with endogenous xenin plasma peaks and induced by exogenous xenin

Xenin, a recently discovered peptide produced by specific endocrine cells of the duodenal mucosa, has shown exocrine, endocrine and motility effects in the gastroenteropancreatic system in animal experiments. The aim of the present investigation was to study the role of xenin in the regulation of duodenojejunal motility of humans. Twenty-nine healthy volunteers from the hospital staff gave informed consent to participate in this investigation. In 20 volunteers, we determined plasma concentrations of immunoreactive xenin at 15 min intervals over a mean time period of 8 h fasting and recorded the interdigestive motor activity of the duodenojejunum. In a double-blind randomized crossover study on other nine subjects, synthetic xenin in a dose of 4 pmol kg-1 min-1 or placebo was infused for 10 min intravenously in the interdigestive period and postprandially after a liquid meal. Duodenojejunal motility was recorded simultaneously. Predefined interdigestive xenin plasma peaks were found to be significantly associated with the phases III of the migrating motor complex. In the interdigestive period, xenin induced a premature phase III activity in each volunteer; this was followed by a second phase III in five out of nine subjects. In the postprandial state, xenin significantly increased contraction frequency and the percentage of aborally propagated contractions. These findings suggest a role of the peptide hormone xenin in modulating interdigestive and postprandial duodenojejunal motility in humans.     

Intragastric acidification inhibits motilin-induced phase III activity in humans

In a randomized, placebo-controlled crossover design we studied the effect of gastric acidification on motilin-induced interdigestive antropyloroduodenal motility. Ten healthy volunteers participated in the study consisting of four experiments. Each experiment started after a spontaneous occurring phase III and consisted of intragastric infusion of either saline or acid (0.08 mol L(-1) HCl) for 90 min and intravenous infusion of either saline or motilin (4 pmol kg(-1) min(-1)) for 30 min. Antropyloroduodenal motility and pH were recorded continuously for 240 min. Reoccurrence of phase III was significantly (P < 0.05) earlier during intragastric saline-intravenous motilin infusion compared with control (intragastric saline-intravenous saline), 52 min (range 25-79) and 113 min (84-141) respectively. This effect was completely abolished during intragastric acid-intravenous motilin infusion, 112 min (82-142). The percentage of phase III of antral origin was significantly (P < 0.05) higher during intragastric saline-intravenous motilin infusion (90%) compared with control (30%). The mean area under the contraction (AUC) for phase II was significantly (P < 0.05) lower during intragastric saline-intravenous motilin infusion and intragastric acid-intravenous saline infusion compared with control. It is concluded that in humans intragastric acidification inhibits the effect of motilin on antroduodenal motility, decreases the AUC of antral phase II contractions and delays the occurrence of phase III of the migrating motor complex.     

Effect of truncal vagotomy on gallbladder bile kinetics in conscious dogs

Previous studies on the effects of vagotomy on gallbladder (GB) motility have yielded conflicting results. The aim of this study was to evaluate the effects of vagotomy on GB motility and bile kinetics using a new method. Twelve dogs were divided into two groups of six (control and pyloroplasty) and, 4 weeks later, underwent truncal vagotomy. A catheter secured in the GB fundus was used to monitor GB volume. After injecting polyethylene glycol (PEG) into the GB, combined measurements of GB volume and PEG concentration enabled GB emptying and bile kinetics to be estimated. Seven and five of the 12 vagotomized dogs were classified as having large and normal fasting GB volumes, respectively. Postprandial GB emptying was impaired when the fasting GB volume was enlarged. In the fasting state, bile kinetics of vagotomized dogs were significantly smaller than the control values. The emptying ability of the GB of vagotomized dogs with large fasting GB volumes was reduced considerably both in the postprandial and the fasting states. Such retention of bile in the GB after vagotomy may facilitate cholesterol crystal nucleation and stone growth.     

Role of Peptide YY in Intestinal and Gallbladder Motility in Dogs

The purpose of this study was to characterize the action of exogenous PYY, an ileocolonic peptide released by fatty meal, and that released by Heal perfusion with oleate on intestinal and gallbladder motility patterns and the posssible role of the adrenergic pathway in this action. Dogs were equipped with chronic duodenal electrodes for recording myoelectric activity and with a cannula in the gallbladder fundus for measuring the gallbladders intraluminal pressure and volume and calculating its motility index (MI) and emptying rate. After intravenous infusion of PYY, there was a dose-dependent prolongation of the migrating motor complex (MMC) interval and almost complete abolition of the contractions and emptying of gallbladder during the duodenal activity front. After meat feeding or during intravenous infusion of cerulein, 50 pmol/(kg · h), the MMC was interrupted and replaced by irregular spike activity, accompanied by a marked increase in the gallbladder MI and about 80% to 90% reduction of its volume. PYY, 200 pmol/(kg · h), reduced significantly the meal- or cerulein-induced duodenal spike activity but failed to affect the MI and volume of the gallbladder. Similar changes in fasted and fed patterns of motility were observed after Heal oleate (16 mM/h), producing plasma PYY levels in a range similar to that observed after infusion of exogenous PYY. The inhibitory effects of PYY or Heal fat on intestinal myoelectric activity were reversed in part by α-adrenergic blockade (phentolamine). We conclude that exogenous PYY or endogenous hormone released by Heal oleate inhibits the interdigestive and postprandial motility pattern of the small bowel but does not affect gallbladder motility, and that the inhibition of intestinal motility involves, at least in part, the adrenergic pathway.     

Gastrointestinal peptides,gastrointestinal motility,and anorexia of aging in frail elderly persons

Background The mechanisms involved in anorexia in frail elderly people remain unclear. The objective of this study was to establish whether fasting and postprandial levels of gastrointestinal peptides, gastrointestinal motility, and hunger are modified by age and frailty. Methods Three groups of subjects were studied: (a) frail elderly (>70 years) persons, (b) non‐frail elderly (>70 years) persons, and (c) healthy adults (aged 25–65 years). After an overnight fast, participants ingested a 400 Kcal liquid meal and appetite, hormonal, and gastrointestinal responses were monitored during early (0–60 min) and late (60–240 min) postprandial periods. Key Results Frail persons showed poor nutritional status, sarcopenia, and almost absence of hunger during fasting and postprandial periods. Older persons presented higher levels of glucose and insulin during fasting, enhanced postprandial CCK release in early postprandial period and postprandial hyperglycemia and hyperinsulinemia, but similar ghrelin levels than younger adults. Ultrasound scan showed that the fasting antral area was higher and antral compliance lower in old persons. The paracetamol absorption test showed enhanced postprandial gastric emptying in the frail. Non‐gallbladder contractors showed no CCK peak in younger and non‐frail groups, but the same high CCK peak as contractors in the frail. Conclusions & Inferences Frailty was associated with anorexia, risk of malnutrition, and sarcopenia. Frail persons showed impaired gastric motility (larger antral area at rest, impaired antral compliance, and enhanced postprandial emptying), impaired gallbladder motility, and fasting and/or postprandial alterations in CCK, glucose, and insulin release. Further studies are needed to determine if these factors may contribute to anorexia of aging in frail persons.     

Meal-induced secretion of gastrointestinal regulatory peptides is not affected by sleep

The mechanisms responsible for the disruption of the migrating motor complex (MMC) by feeding are not fully understood. Sleep reduces the duration of the postprandial or fed pattern of motility in the intestine. This study was set out to determine if this effect is associated with sleep-induced changes in the secretion of regulatory peptides in response to food. Methods: Duodenojejunal motility was studied in 15 healthy ambulant subjects for 2 consecutive days. On one day identical solid meals were consumed in the morning and late in the evening, the latter followed by sleep. On the other day, identical liquid meals were infused into the stomach and the duodenum in the morning and late in the evening, the latter after the onset of sleep. Plasma concentrations of gastrin, neuro­tensin, peptide YY (PYY), pancreatic polypeptide (PP), motilin and glucose were monitored before and after meals.
Sleep significantly shortened the duration of the fed pattern after the solid meal and even more so after the liquid meal. The plasma concentrations of all peptides, except motilin, increased significantly following each meal. Blood glucose levels rose after each meal, the changes being similar with all meals.
Food-induced gastrointestinal regulatory peptides secretion and intestinal absorption of glucose are not affected by sleep. The vagal response to a meal, as indicated by PP release, is intact during sleep. The results support the importance of neural mechanisms in the modulation of the postprandial pattern of intestinal motility.     

GLP-1 regulates gastroduodenal motility involving cholinergic pathways

Abstract  The gut-born incretin hormone glucagon-like peptide-1 (GLP-1) delays gastric emptying. To elucidate the mechanisms by which GLP-1 affects gastroduodenal motility and glycaemia, we studied the effects of exendin(9–39), a potent GLP-1 receptor antagonist, on gastroduodenal motility and pancreatic hormones. In this randomized, double-blind, placebo-controlled, four-arm, cross-over trial, 10 healthy volunteers were studied during the interdigestive period followed by duodenal perfusion of a mixed liquid meal (250 kcal). On four separate days, exendin(9–39), atropine, exendin(9–39) + atropine or saline were infused intravenously. Antro-pyloro-duodenal and fundic motility were assessed. The compliance of the proximal stomach was determined by isobaric distensions. During fasting, exendin(9–39) did not influence proximal gastric volume, pyloric tone, and duodenal contractility. Exendin(9–39) significantly increased antral waves only in the absence of atropine. During duodenal meal perfusion, exendin(9–39) significantly reduced proximal gastric volume accommodation, abbreviated postprandial antral inhibition, reduced the postprandial increase in pyloric tone, and reduced gastric compliance. Atropine abolished the effects of exendin(9–39) on gastric volume accommodation but did not affect its effects on postprandial antroduodenal motility and on gastric compliance. Exendin(9–39) increased fasting and postprandial glycaemia and plasma glucagon but not insulin concentrations. Atropine did not affect GLP-1 secretion. Cholinergic mechanisms mediate the effects of GLP-1 on postprandial gastric accommodation but not on antro-pyloro-duodenal motility. GLP-1 reduces fasting and postprandial glycaemia, in part by reducing glucagon secretion.     

Gastric myoelectrical and antroduodenal motor activity in patients with achalasia

Achalasia is a primary motor disorder of the oesophagus, in which the myenteric plexus is involved. However, abnormalities in other parts of the digestive tract have also been described in achalasia. Whether gastric myoelectrical and duodenal motor activity in these patients is also affected is unknown. Therefore, interdigestive and postprandial gastric myoelectrical and antroduodenal motor activity were studied in 11 patients with achalasia, using electrogastrography (EGG) and stationary antroduodenal manometry.
Electrogastrographically, no differences were found in the gastric frequency, incidence of dysrhythmias and postprandial/fasting power ratio. In the interdigestive state a lower propagation velocity of phase III episodes was found in the achalasia patients, but other parameters were unaltered. Postprandially, no differences were found in the number of pressure waves, in the amplitude of pressure waves or in antro-duodenal coordination.
We conclude that gastric myoelectrical activity and antral motor activity in patients with achalasia is normal, suggesting an intact extrinsic and intrinsic neural innervation of the distal stomach. Although postprandial duodenal motility is normal, a lower propagation velocity of phase III suggests involvement of the small intestine in achalasia.     

Factors in the Control of Interdigestive and Postprandial Myoelectric Patterns of Canine Jejunoileum: Role of Extrinsic and Intrinsic Nerves

Our aim was to determine the roles of extrinsic and intrinsic (enteric) neural continuity to the jejunoileum in control of postprandial and fasting motility patterns. Four groups of dogs were prepared: control, neurally intact; intrinsic transection, distal duodenal transection to disrupt intrinsic myoneural continuity with jejunum; extrinsic transection, transection of all extrinsic nerves to jejunoileum; and intrinsic/extrinsic transection, disruption of both intrinsic myoneural and extrinsic neural continuity to jejunoileum. Duodenal and jejunal electrodes were placed to monitor motility. After 2 weeks, the dogs were studied while fasting, after meals, and during intravenous infusions of cholecystokinin octapeptide at 0.5μg/(kg · h) and pentagastrin at 2μg/(kg · h). During fasting, although the migrating motor complex (MMC) occurred in each region, coordination between duodenum and jejunoileum was disrupted in intrinsic/extrinsic transection dogs, but only partially in intrinsic transection dogs. Small meals (50 g of liver) interrupted the duodenal MMC in all groups and the jejunoileal MMC only in control dogs. A larger (500-g) meal disrupted the MMC in both regions for comparable durations in all groups. Cholecystokinin octapeptide and pentagastrin inhibited the MMC in duodenum and jejunoileum in all groups. Both intrinsic myoneural and extrinsic neural continuity play a role in regional coordination of interdigestive and digestive gut motility. Both hormonal and neural factors (central, enteric) participate in the regulation of onset of postprandial motor patterns.     

Comparison of small‐bowel motility of the human jejunum and ileum

Background Knowledge about human cyclic fasting motility (MMC) and the postprandial response is mostly based on manometric findings in the upper small intestine. Hardly any data exist on human ileal motility, as the acquisition of data has been limited by methodological concerns. The aim was to study human jejunal and ileal motility in an optimized manometric setting. Methods Solid‐state 24‐h‐manometry was performed in the jejunum and ileum of healthy individuals, applying a strict protocol for fasting, resting, and the consumption of a standardized meal. Both visual qualitative and validated computerized quantitative contraction and propagation analysis were performed. Key Results MMC occurs in similar frequency in the jejunum and ileum, but it was significantly shorter in the jejunum at night. By many characteristics, ileal motility was less intense and propagative than jejunal: less migrating clustered contractions, and slower propagation velocity and shorter distance in phases II and III, and postprandially – possibly slowing and enhancing nutrient absorption. Prolonged propagated contractions in some individuals were identified as a unique ileal propulsive pattern. Postprandially, an abrupt conversion to a digestive motility pattern occurs simultaneously independent of the region. Conclusions & Inferences We found similar basic phenomena of fasting and postprandial motility in the jejunum and ileum of healthy humans. However, different calibration of propagative and contractile activity and special motor events in the ileum may account for a different physiological role in digestion. Future studies of small‐bowel motility in healthy and diseased subjects focusing on segmental differences of proximal and distal intestine may be rewarded.     

Differential effects of motilin on interdigestive motility of the human gastric antrum, pylorus, small intestine and gallbladder

Motilin was infused in this study with the aim of examining refractory characteristics for motilin stimulation of antral phase III and fasting gallbladder emptying. Moreover, interdigestive pyloric and small intestinal motility from duodenum to ileum were studied, as these may be target organs for motilin. Eight fasting, healthy male volunteers received, on separate subsequent days, repeated infusions of 13leucine-motilin (8 pmol (kg min)(-1) for 5 min) or saline at 30 min after phase IIIs in the duodenum. Interdigestive motility of the antrum, pylorus, duodenum, jejunum and ileum was measured for maximum 10 h by using a 21-lumen perfused catheter. Gallbladder motility was measured by ultrasonography. Motilin infusions induced antral phase IIIs, but only after a preceding phase III of duodenal origin. Under this condition, time-interval to phase III at the duodenal recording site was 30 +/- 13 (SEM) min after motilin, compared with 79 +/- 14 min after saline (P < 0.01), and compared with 121 +/- 13 min for motilin infusion following an antral phase III (P < 0.001). Motilin did not affect small intestinal motility or isolated pyloric pressure waves (IPPWs). However, the number of IPPWs was significantly affected by the origin of the preceding phase III, irrespective of whether motilin or saline was infused. Gallbladder volume decreased significantly within 10 min after each motilin infusion. We conclude that this study clearly demonstrates differential regional effects of motilin. Motilin initiates antral phase IIIs, but stimulation is subject to a refractory period which is clearly prolonged after a preceding antral phase III. Motilin induced gallbladder emptying, however, is not subject to a refractory state. Small intestinal phase IIIs as well as pyloric IPPWs are not affected by motilin.     

High interdigestive and postprandial motilin levels in patients with the irritable bowel syndrome

Motilin shows cyclic variation with the different phases of the migrating motor complex (MMC). Altered motilin levels have been found in irritable bowel syndrome (IBS) patients, but in these studies motilin levels were analysed without the knowledge of the phases of MMC. We included 13 healthy controls (HC) and 24 patients with IBS [12 diarrhoea-predominant (IBS-D) and 12 constipation-predominant (IBS-C)]. We performed interdigestive and postprandial antroduodenojejunal manometry and blood samples for analysis of motilin were drawn. Group differences in plasma levels of motilin were analysed during mid-phase II, just before the start of phase III (pre-III), during phase I, immediately before the meal and 30 and 60 min after the 500 kcal mixed meal. Higher motilin levels were observed in IBS vs HC in both the interdigestive and postprandial periods (P < 0.05). No significant differences between IBS-C and IBS-D were observed. The cyclic variation of motilin during MMC and the meal response was similar in IBS and controls. IBS patients, irrespective of the predominant bowel habit, demonstrate higher motilin levels than HCs in all phases of the MMC and also after a meal. These findings may bear some pathophysiological importance in IBS and relate to the gastrointestinal dysmotility often seen in these patients.     

Reproducibility of antroduodenal motility during prolonged ambulatory recording

Ambulatory recording of antroduodenal manometry is a novel technique with several advantages over standard stationary manometry recording. Although the feasibility of this technique in clinical practice has been demonstrated, reproducibility of antroduodenal motility recorded by means of ambulatory manometry has not been investigated. To test whether antroduodenal motility recorded by ambulatory manometry is reproducible, we performed two 24-h ambulatory antroduodenal manometry recordings in 18 healthy subjects according to an identical protocol with a 1-week interval. Motility was recorded with a five-channel solid-state catheter. Postprandial motility was recorded after consumption of two test meals and interdigestive motility was recorded nocturnally. Postprandial antroduodenal motor characteristics were identical between the separate recordings. The number and duration of nocturnal cycles of the interdigestive migrating motor complex were also in the same range. Phase III characteristics in general were not different between the two recordings. Only minor alterations were observed in the duration of phase III motor fronts with duodenal onset and in the number of interdigestive cycles concluded by duodenal onset phase III. Parameters obtained by qualitative analysis were comparable between the two recordings. The antroduodenal motility pattern, when measured by ambulatory recording with solid state catheters under standardized conditions, is very reproducible.