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PubMed1990

Relationship between enteric migrating motor complex and the sleep cycle.

To address the question of synchrony between two major biorhythms with a similar periodicity, the cortical rapid eye movement (REM)/non-REM sleep cycle and the enteric migrating motor complex (MMC cycle), we recorded upper small bowel motor activity and sleep activity during nocturnal and diurnal sleep in six healthy subjects. Motility was measured continuously using a fine (2.2 mm OD) and relatively comfortable nasojejunal probe with two pressure-sensitive microtransducers positioned under fluoroscopic control on either side of the ligament of Treitz. Sleep stages were recorded while the subjects slept in a sleep laboratory. Each subject was studied twice; once during normal nocturnal sleep and then after acute reversal of sleep by advancing the time of going to bed by 4 h each night for three nights. The total duration of sleep was similar for diurnal and nocturnal sleep. There was a significantly higher number of REM episodes (P less than 0.001) and REM sleep stage shifts (P less than 0.02) during diurnal (reversed) sleep. During sleep (both diurnal and nocturnal) there was a significant reduction in the MMC cycle length (P less than 0.02, P less than 0.03) and the duration of phase II of the MMC (P less than 0.009, P less than 0.02). The distribution of MMCs among sleep stages and REM sleep was consistent with a random distribution. These data show that periodic activity in the gut is modulated by the presence or absence of sleep, but they also are consistent with the hypothesis that the two cycles are independent and that one is not contingent upon the other.

Adult↗

PubMed1998

Migrating motor complex cycle duration is determined by gastric or duodenal origin of phase III.

The migrating motor complex (MMC) shows large variations within an individual and between individuals. This study aimed to investigate, with respect to this variability, the importance of gastric or duodenal origin of phase III activity. Interdigestive 6- to 10-h stationary antroduodenal motility recordings of 19 healthy male subjects were analyzed for MMC cycle durations and duration of phases I, II, and III, all with respect to the place of origin of each phase III. Data are given for the duodenal recording site as means +/- SE. Mean MMC cycle duration was 117.3 +/- 13.9 min, regardless of the place of origin of phase III. Seventy-two phase III cycles were observed in total, 35 and 37 starting in the "antrum" and duodenum, respectively. After a phase III of "antral" origin, MMC cycle duration was 156.1 +/- 11.0 min, significantly longer than MMC cycle duration following a phase III of duodenal origin, 80.5 +/- 10.7 min (P < 0.001). Phase III duration was longer when of "antral" origin than when starting in the duodenum (7.6 +/- 0.4 and 5.3 +/- 0.4 min, respectively; P < 0.001). MMC cycle duration and duration of phases I, II, and III depend on the place of origin of phase III ("antral" or duodenal) and on the origin of the preceding phase III. This factor explains part of the MMC variability observed within individuals. Mean MMC cycle duration in healthy subjects or patients should therefore also include information on the origin of phase III.

Adult↗

PubMed2000

Effect of melatonin on motility pattern of small intestine in rats and its inhibition by melatonin receptor antagonist S 22153.

Melatonin is synthesized during the night by the pineal gland. Recently, melatonin binding sites have been identified in the gut. Despite few studies, the physiological role of melatonin in gut function remains unclear. The objective of the present study was to investigate the effects of melatonin in the regulation of intestinal motility by using the melatonin receptor antagonist S 22153 in rats. Twenty-four male Wistar rats (400 +/- 25 g) were equipped with intraparietal electrodes along the small intestine. Rats were subjected to a 12:12 hr light:dark schedule. During the dark phase, intestinal migrating motor complexes (MMCs) frequency increased (P < 0.05) by 20% in the duodenum and in the jejunum compared with daylight. This effect is due to a significant reduction in the irregular spiking activity (ISA) of MMCs. Concurrently, at night, the duration of the postprandial motor response is reduced by 30% in the duodenum and 50% in the jejunum and ileum. The administration of S 22153 (2 mg/kg sc) at night suppressed these nocturnal variations and restored the daylight values. In contrast, S 22153 was ineffective during daylight whatever the digestive state. Administration of melatonin (1 mg/kg iv) during the preprandial state, 3 hr after light onset, decreased (-80%) the duration of the ISA of MMCs at the three intestinal levels. During the satiety phase, melatonin administered 10 min before or 15 min after food onset induced the appearance of a transitory preprandial-like motor profile in the entire small intestine. In contrast, when administered at the end of the meal it was ineffective. Preprandial and postprandial melatonin effects were prevented by S 22153 pretreatment. In conclusion, these findings reveal, first, that endogenous melatonin is physiologically involved in the pre- and postprandial changes of intestinal motility at night. Second, exogenous melatonin produces pharmacological effects on pre- and postprandial intestinal motility. In both cases, the action of melatonin corresponds to an inhibition of ISA and a reinforcement of the cyclic MMC pattern.

Action Potentials↗

PubMed1996

M1-muscarinic mechanisms regulate interdigestive cycling of motor and secretory activity in human upper gut.

We determined the influence of M1-muscarinic pathways in modulating temporal cycling of motor and secretory activity in the fasting upper gut. Eight healthy subjects were studied on two separate days, following a double-blind, randomized protocol. Antroduodenal motility (migrating motor complex, MMC), pancreatic exocrine secretion (amylase, lipase, trypsin, chymotrypsin), and plasma levels of associated hormones [motilin, pancreatic polypeptide (PP)] were monitored for two consecutive cycles during background infusion of placebo or telenzepine, a selective M1-muscarinic receptor antagonist. On placebo days, pancreatic enzymes and hormones cycled in synchrony with motor activity, as expected. During M1 blockade, duodenal output of each enzyme was decreased by 85-90% in phase I and by > 90% in phase III. Similarly, plasma concentrations of hormones were decreased during all phases and cycling was absent. Despite the loss of these putative influences, intestinal motility continued to cycle, albeit in an altered fashion. Intermittent phase II activity was replaced by phase I quiescence, while phase III-like fronts were diminished (contraction frequency, amplitude, propagation velocity reduced 30-60%, duration not altered) but recurred at expected intervals (cycle length 105 +/- 14 min vs 109 +/- 12 in placebo). Gastric motor activity was virtually abolished. These data suggest or extend several working hypotheses: (1) Motilin is released and/or acts via cholinergic (M1-muscarinic) pathways to initiate antral, but not duodenal, phase III activity. (2) M1 receptors mediate all components of the gastric MMC and phase II activity throughout the gut, but intestinal phase III activity arises via alternate pathways. (3) M1-muscarinic mechanisms regulate interdigestive cycling of pancreatic enzymes and PP. (4) Secretions from the endocrine/exocrine pancreas are not primary mediators of intestinal motility.

Adult↗

PubMed2003

Migrating motor complexes do not require electrical slow waves in the mouse small intestine.

We have investigated whether migrating motor complexes (MMCs) are impaired or absent in the small intestine of W/Wv mutant mice, which lack pacemaker interstitial cells of Cajal (ICC) and electrical slow waves. The intracellular electrical and mechanical activities of the small intestines of wild-type (+/+) and W/Wv mutant mice were recorded. Electrical recordings from circular muscle cells confirmed the absence of slow waves in W/Wv mice, whereas slow waves were always recorded from +/+ muscle cells. Spontaneous phasic contractions were recorded from W/Wv muscles in the absence of slow waves, but these events occurred at a lower frequency than in +/+ tissues. MMC activity was recorded consistently from the ileum of +/+ mice, and normal MMCs were also recorded from W/Wv mice. MMCs in both +/+ and W/Wv mice were abolished by tetrodotoxin (1 microM), hexamethonium (300 microM) or atropine (1 microM), suggesting that the neural control mechanisms responsible for MMCs in +/+ mice are intact and are responsible for MMCs in W/Wv mice. Transmural nerve stimulation demonstrated intact inhibitory and excitatory neural regulation of W/Wv intestinal muscles. Prolonged trains of cholinergic motor nerve stimulation failed to activate slow waves in the intestinal muscles of W/Wv mice. Our findings show that the generation and directional propagation of MMC activity in mouse small intestine does not require slow-wave activity or an intact network of myenteric ICC. The generation and propagation of MMCs appear to be an intrinsic capability of the enteric nervous system and are not related to slow waves or the gradient in slow-wave frequency.

Animals↗

PubMed2006

Development of colonic motility in the neonatal mouse-studies using spatiotemporal maps.

Colonic migrating motor complexes (CMMCs) are spontaneous, anally propagating constrictions, repeating every 3-5 min in mouse colon in vitro. They are regulated by the enteric nervous system and may be equivalent to mass movement contractions. We examined postnatal development of CMMCs and circular muscle innervation to gain insight into mechanisms regulating transit in the maturing colon. Video recordings of mouse colon in vitro were used to construct spatiotemporal maps of spontaneous contractile patterns. Development of nitric oxide synthase (NOS) and cholinergic nerve terminals in the circular muscle was examined immunohistochemically. In adults, CMMCs appeared regularly at 4.6 +/- 0.9-min intervals (n = 5). These intervals were reduced by inhibition of NOS (2.7 +/- 0.2 min; n = 5; P < 0.05). CMMCs were abolished by tetrodotoxin (n = 4). CMMCs at postnatal day (P)10 were indistinguishable from adult. At birth and P4, CMMCs were absent. Instead, small constrictions that propagated both orally and anally, "ripples," were seen. Ripples were unaffected by tetrodotoxin or inhibition of NOS and were present in Ret(-/-) mice (which lack enteric neurons) at embryonic day 18.5. In P6 mice, only ripples were seen in control, but NOS inhibition induced CMMCs (n = 8). NOS terminals were abundant in the circular muscle at birth; cholinergic terminals were sparse but were common by P10. In mouse, myogenic ripples are the only mechanism available to produce colonic transit at birth. At P6, neural circuits that generate CMMCs are present but are inhibited by tonic activity of nitric oxide. Adult patterns appear by P10.

Animals↗

PubMed1998

Interdigestive antroduodenal motility and gastric acid secretion.

BACKGROUND: In humans, interdigestive acid secretion and antroduodenal motility are closely related with cyclic variations in acid secretion, synchronous with the various phases of the migrating motor complex (MMC). Duodenal acidification inhibits antral motility, but little is known about the effect of acute acid inhibition on antroduodenal motility. AIM: To study the effect of acute acid inhibition on antroduodenal motility. SUBJECTS: Ten healthy volunteers (four men and six women: age range 20-31 years). METHODS: Antroduodenal motility (perfusion manometry) and gastric acid secretion (continuous aspiration with recovery marker) were measured simultaneously. Each subject was studied twice in random order during (1) intravenous infusion of saline for one-two complete MMC cycles and (2) during acute acid inhibition with intravenous famotidine (bolus 20 mg, continuous infusion 4 mg/h) for one-two complete MMC cycles or at least 240 min. RESULTS: In the saline study, acid output in phase III (2.1 +/- 0.3 mmol/10 min) and late phase II (1.7 +/- 0.2 mmol/10 min) was significantly (P<0.05) increased over early phase II and phase I (1.2 +/- 0.2 and 1.2 +/- 0.2 mmol/10 min, respectively). Famotidine increased gastric pH to above pH 6 within 30 min. After acid inhibition, duration of MMC cycle during famotidine (106 +/- 8 min) was not significantly different from the saline experiment (133 +/- 14 min). Phase distribution of the MMC cycle was not significantly different between famotidine (I, II and III: 12 +/- 3, 82 +/- 3 and 5 +/- 1%) and saline (I, II and III: 13 +/- 3, 83 +/- 3 and 4 +/- 1%). CONCLUSIONS: Gastric acid secretion varies cyclically with interdigestive antroduodenal motility. Acute acid inhibition with intravenous famotidine does not significantly affect interdigestive antroduodenal motility.

Adult↗

PubMed1997

Ca2+ channel blockade by verapamil inhibits GMCs and diarrhea during small intestinal inflammation.

The aim of this study was to investigate whether the blockade of L-type Ca2+ channels with verapamil suppresses giant migrating contractions (GMCs) and therefore diarrhea during small intestinal inflammation. Small intestinal inflammation was induced by infection with the nematode Trichinella spiralis. T. spiralis infection alone significantly increased the frequency of GMCs and decreased the frequency of phase III activity in the small intestine for 9 days. The increased frequency of GMCs was associated with diarrhea. Immunohistochemical staining with specific antibodies indicated that the number of neutrophils and mast cells increased significantly in the jejunal lamina propria during T. spiralis infection. Only the neutrophils increased significantly in the muscularis externa of the jejunum. Myeloperoxidase (MPO) activity increased significantly in the jejunal and ileal lamina propria. Daily verapamil administration during T. spiralis infection significantly reduced the frequency of GMCs and diarrhea but had no further significant effect on the already reduced frequency of phase III activity. Verapamil administration, however, did not reduce MPO activity or immunocyte infiltration in the jejunum or ileum. We conclude that blockade of L-type Ca2+ channels selectively reduces the frequency of GMCs and therefore diarrhea during small intestinal inflammation. The decreased frequency of GMCs is not secondary to a reduction in the inflammatory response.

Animals↗

PubMed1994

Mechanisms coordinating gastric and small intestinal MMC: role of extrinsic innervation rather than motilin.

We have investigated the role of vagal and efferent adrenergic innervation coordinating the gastric and small intestinal migrating motor complexes (MMCs) after removal of the pylorus, duodenum, and upper jejunum in three dogs. The cervical vagus nerves were previously isolated in bilateral skin loops to permit reversible cooling blockade of the vagi. Pharmacological alpha- and beta-receptor blockade was accomplished by bolus intravenous injection of phentolamine and propranolol followed by intravenous infusion of the combined drugs. Gastric and upper jejunal MMC-like activity was initially absent after bowel resection but reappeared after 1-4 mo with the gastric and jejunal MMC-like activities coordinated as if the jejunum were the duodenum. Motilin peaks were absent. All gastric contractions were abolished by vagal blockade. Pharmacological adrenergic blockade immediately induced an intense burst of contractile and electrical activity in the stomach, which propagated to the distal ileum. This phase III-like burst was followed by ongoing intermittent bursts of contractile and electrical activity in the stomach and small intestine, lasting throughout the blockade, without further MMC-like activity. Vagal cooling blockade in combination with adrenergic blockade did not restore gastric MMC-like activity but abolished or decreased the number of gastric contractions, with the reappearance of the small intestinal MMC. Atropine boluses abolished all control and adrenergic blockade-induced stomach and small intestinal contractile and electrical activity. In conclusion, after duodenectomy, the gastric MMC-like activity that is reestablished and is coordinated with the small intestinal MMC is vagally dependent and cholinergic, but its cyclical nature requires adrenergic efferent pathways. Under these circumstances, coordination of the gastric and jejunal MMCs appears to require extrinsic innervation.

Animals↗

PubMed1992

The effects of omeprazole on interdigestive motility and early postprandial levels of gastrin and secretin.

Ten healthy men participated in a crossover study, and the experiments took place after 10 days of treatment (40 mg omeprazole every morning). Blood samples were drawn at fixed intervals during a complete migrating motor complex (MMC) cycle. The manometric pressure tube was removed after passage of the second duodenal phase III, and an omelet (1400 KJ) tagged with 99mTc was ingested, followed by 150 ml of water tagged with 111In-diethylenetriaminepentaacetic acid. Mean plasma gastrin (pmol/l) in phases I, II, and III in the omeprazole group was 18.8, 23.3, 19.9, respectively. The corresponding figures for the placebo group were 9.3, 9.6, 9.5, respectively. All mean values for the omeprazole group were significantly higher (p less than 0.01). Mean plasma gastrin in the omeprazole group was significantly higher in phase II than in phase I (p less than 0.05). Mean plasma secretin (pmol/l) in phases I, II, and III in the omeprazole group was 1.6, 1.4, 1.1, respectively. The corresponding figures for the placebo group were 2.0, 1.7, 2.2, respectively. Mean plasma secretin in the omeprazole group was significantly lower in phases I and III (p less than 0.05). The mean incremental integrated postprandial gastrin response (pmol.30 min/l) was significantly higher in the omeprazole group (475.0 versus 97.5) (p less than 0.05). The immediate postprandial mean value of secretin was significantly lower in the omeprazole group (p less than 0.05). We conclude that 40 mg omeprazole elicits i) a phase-related increase in fasting plasma gastrin, ii) a decrease in secretin in phases I and III, iii) an augmented meal-stimulated gastrin response, and iv) a secretin response characterized by a significantly lower mean in the immediate postprandial period.

Adult↗

PubMed2002

Gastric phase 3 motility after pylorus-preserving pancreatoduodenectomy.

OBJECTIVE: To analyze factors affecting the recovery course of phase 3 activity of the gastric migrating motor complex after pylorus-preserving pancreatoduodenectomy (PPPD) and investigate effects of the recovery of gastric phase 3 on gastric emptying after feeding. SUMMARY BACKGROUND DATA: Whether early recovery of gastric phase 3 during fasting would predict early recovery of the fed-state gastric emptying function after PPPD has not been well documented. METHODS: Manometric recording from the gastric antrum was repeated at a weekly interval until the first appearance of gastric phase 3 in 57 patients after PPPD. Twenty-three clinical parameters were assessed as possible factors affecting the recovery course of gastric phase 3 by simple and multiple regression analyses. A gastric emptying study after feeding of a test meal was performed by the acetaminophen method and the values were compared between patients with and without gastric phase 3 after PPPD. RESULTS: The mean period before the first appearance of gastric phase 3 was 38 days. Among 23 parameters, only lymph node dissection along the hepatoduodenal ligament significantly delayed recovery of gastric phase 3 after PPPD by univariate and multivariate analyses. The presence or absence of gastric phase 3 in the early postoperative period did not influence gastric emptying after feeding in the intermediate period after PPPD. CONCLUSIONS: Avoiding lymph node dissection along the hepatoduodenal ligament, if applicable, may contribute to early recovery of gastric phase 3 after PPPD. The recovery state of gastric phase 3 during fasting, however, is not necessarily consistent with the degree of improvement of gastric emptying after feeding.

Adult↗

PubMed1996

The relationship between gut hormone secretion and gastric emptying in different phases of the migrating motor complex.

BACKGROUND: No studies are available on the relationship between the response of gut hormones and gastric emptying in different phases of the migrating motor complex. This study examined whether basal gut hormone concentrations in plasma before food ingestion are predictors of emptying characteristics and whether different hormone secretion patterns are associated with specific alterations in emptying rate. METHODS: Twelve healthy men were examined on two occasions: one with meal ingestion in phase I and the other with meal ingestion in phase II. The meal consisted of an omelette labelled with 99mTc followed by 150 ml water labelled with 111In. Plasma concentrations of gastrin, cholecystokinin, motilin, and peptide YY were measured in the fasting state, immediately after food ingestion, and at 15-min intervals in the postprandial period. RESULTS: New findings from the present study include a higher incremental integrated postprandial motilin response in phase I than in phase II (998 pmol/l*30 min (495 to 2010) versus 210 pmol/l*30 min (-270 to 2323), p < 0.05), and a linear relationship between median total integrated motilin response and solid emptying at 120 min in phase I (Rs = 0.58; p < 0.05). Furthermore, in phase I a linear relationship between total integrated area of cholecystokinin and solid emptying at 120 min was demonstrated (Rs = 0.62; p < 0.05). CONCLUSION: The findings from the present investigation have to be considered in the future design of studies that focus on postprandial release of gastrointestinal hormones. The transition from phase III to phase I is a reproducible and easily recognized pressure event. Therefore, we recommend the use of food ingestion immediately after termination of duodenal phase III.

Adult↗

PubMed1995

Migrating motor complex and sleep in health and irritable bowel syndrome.

The human migrating motor complex (MMC) and sleep cycle have a similar periodicity, and there is some contention as to whether these biorhythms are linked. In irritable bowel syndrome (IBS), episodes of intestinal dysmotility have been described almost exclusively during wakefulness, but IRS patients often complain of poor sleep, and it has been suggested that IBS patients have increased rapid eye movement (REM) sleep. This study sought to identify any associations between sleep stage and small intestinal motility and any objective sleep abnormalities in IBS. Nocturnal motility was recorded from six small intestinal sensors mounted on a fine nasoenteric catheter in eight IBS patients and 10 healthy volunteers. Polysomnography to determine sleep stage was recorded simultaneously. The proportions of time awake, in non-REM and REM sleep was similar in controls and IBS. REM latency did not differ between the two groups despite increased depression in the IBS patients (Hamilton Depression Rating of 8.3 +/- 1.7 in IBS, 3.0 +/- 0.7 in controls, P < 0.01). Nocturnal motility was similar, with phase I occupying most of the MMC cycles. There was no temporal association between MMCs and sleep stage, with no synchrony of phase III for REM episodes. The mean motility index of 4.5 +/- 0.4 during wakefulness was greater than during all sleep stages (P < 0.05). During non-REM sleep stages 1 and 2, motility index of 3.2 +/- 0.3 was greater than 2.3 +/- 0.2 during stages 3 and 4 (P < 0.05), but similar to motility index of 3.3 +/- 0.4 during REM sleep. This sleep architecture and nocturnal small intestinal motility are normal in IBS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2005

Duodenal acid clearance in humans: observations made with intraluminal impedance recording.

Duodenal acid clearance appears to be involved not only in the pathogenesis of duodenal ulcer disease but also in functional dyspepsia. Duodenal contractile activity can help to maintain neutral pH in the duodenum by mixing acid with bicarbonate or by aborally transporting the acid load. Intraluminal impedance recording, allowing the detection of nonacid liquid boluses, can be carried out concomitantly with antroduodenal manometry and pH recording and may thus provide useful information about the mechanisms involved in duodenal clearance of endogenous acid and volume boluses. Eight H. pylori-negative healthy volunteers were studied with two catheters positioned across the pylorus, allowing the recording of five impedance signals (one antral, one pyloric, and three duodenal) simultaneously with six pressure signals (two antral, one pyloric, and three duodenal) as well as distal antral and proximal duodenal pH. During phase II of the migrating motor complex, which is known to be associated with the highest duodenal acid exposure, each duodenal acidification event (defined as a pH drop >2 pH units) was characterized by its maximal amplitude, duration, temporal relationship with antroduodenal manometric events, and relation to impedance variations. Acid was considered to have been cleared from the duodenum when the preacidification pH was restored (+/-0.2 unit). A total of 164 duodenal pH drops were recorded during the 323 min of phase II recordings. Eleven percent of the duodenal acidification events were short-lived (<10 sec). All of these events were temporally associated with a propagated antroduodenal contraction and a short-lived drop in impedance, suggesting rapid aboral passage of the acid bolus. The long-lived duodenal acidification events lasted a mean of 32 sec (range, 25-66 sec). In 90% of these events an antroduodenal propagated contraction was recorded at the time of onset. Repetitive duodenal contractions followed the onset of the long-lived acidification events in 34% of the cases. These remained present until complete clearance of the acid. In 81% of the long-lived acidification events, recovery of the associated impedance drop occurred simultaneously with the pH recovery, suggesting a complete clearance of the bolus. Less frequently (19%), the duodenal pH recovered while the impedance remained low, suggesting that the bolus was not cleared but neutralized. Interdigestive duodenal acidification events usually last about 30 sec. They evoke duodenal contractions in only one-third of cases. Combined pH and impedance recording makes it possible to distinguish between neutralization of acid boluses and their complete total clearance.

Adult↗

PubMed1997

Endogenous CCK disrupts the MMC pattern via capsaicin-sensitive vagal afferent fibers in the rat.

A meal disrupts migrating motor complexes (MMC) in the rat intestine through stimulation of peripheral cholecystokinin (CCK)-B and central CCK-A receptors. The aim of this study was to determine pathways implicated in postprandial disruption of the MMC mediated by CCK. Sprague-Dawley rats were prepared with electrodes for electromyography in the small intestine, and ablation of vagal afferent C-fibers by capsaicin was carried out. Endogenous release of CCK was induced by oral administration of soybean trypsin inhibitor (SBTI). In control rats SBTI disrupted MMC and generated an irregular spiking activity that lasted longer than 3 h. Intravenous infusion of L-365,260 (2 x 10(-7) mol/kg) but not of L-364,718 (3 x 10(-9) mol/kg) restored the MMC pattern. In capsaicin-treated rats, SBTI did not modify fasting activity. Infusion of CCK octapeptide (CCK-8) at 3 x 10(-9) mol.kg-1.h-1 disrupted the MMC, although the response was quantitatively and qualitatively different from SBTI. The effect was reversed by intravenous infusion of L-364,718 or L-365,260 and intracerebroventricular infusion of L-364,718. In capsaicin-treated rats, the intracerebroventricular or intravenous infusion of L-364,718 inhibited CCK-8 effects. However, the intravenous infusion of L-365,260 did not reverse the MMC pattern. These results suggest that the disruption of the MMC mediated by CCK is due to stimulation of peripheral CCK-B receptors located in vagal afferent fibers. This initiates a reflex including stimulation of central CCK-A receptors. Exogenous CCK also stimulates peripheral CCK-A receptors not located in capsaicin-sensitive vagal afferent fibers.

Afferent Pathways↗

PubMed1995

Absence of correlation between hepatic function and characteristics of migrating motor complexes in the gastrointestinal tract.

BACKGROUND: Cyclic changes in gallbladder filling and emptying during the migrating motor complex (MMC) cycle have been demonstrated by scintigraphy. However, a possible cyclic change in the hepatic function and handling of the pharmacologic agents used for scintigraphy during the MMC cycle could have an influence on these results. The aim of the present study was to investigate the hepatic handling of cholic acid and mebrofenin in relation to the MMCs of the gastrointestinal tract. METHODS: The plasma disappearance rate of 14C-cholic acid and the hepatic uptake and excretion of 99mTc-mebrofenin were examined during phase I and phase II of the MMC in six healthy male volunteers. RESULTS: The plasma disappearance rate of 14C-cholic acid showed a biexponential course with an initial rapid and late slow phase after a bolus injection. There were no significant differences between the initial or late plasma disappearance rate of 14C-cholic acid during phase I as compared with phase II. The results of the time-activity curves from the 99mTc-mebrofenin scintigraphy showed an exponential rapid increase in radioactivity followed by an almost linear slow decrease after a bolus injection. There was no significant difference between phase I and phase II in any of the variables studied. CONCLUSION: The lack of a relationship between hepatic handling of cholic acid and mebrofenin and MMC excludes this as a possible source of error in the investigations of the dynamic function of the enterohepatic circulation and especially gallbladder motility by the use of either cholic acids or iminodiacetic acid derivatives as investigative agents.

Adult↗

PubMed1999

Distension-induced duodenal contractions vary with the phases of the canine interdigestive migrating motility complex.

BACKGROUND: The aim of the study was to evaluate whether the sensitivity for distension-induced contractions in the duodenum varied with the phases of the interdigestive migrating motility complex (MMC). METHODS: Four beagles (12-17 kg) with gastric fistulas were studied by means of perfused low-compliance manometry. A 2.5-cm-long balloon was placed in the third part of the duodenum. Side holes for pressure measurements were placed inside the balloon, 2cm proximal to the balloon, and in the antrum. Two-minute distensions with balloon pressures of 10 cmH2O were repeated in 10-min intervals during 17 MMCs. Twelve MMCs were also recorded without doing distensions. RESULTS: Balloon distension did not affect the duration of phase III and the MMC. In the beginning of phase I, distension did not significantly affect duodenal motility whereas distension induced contractile responses in late phase I, early phase II and late phase II (p < 0.05). The highest increase from the pre-distension to distension period was observed in early phase II (average 4 contractions min(-1)). However, considering the level of pre-distension contraction frequency, the fractional increase was by far the highest in late phase I. In phase III no difference was found between the periods before and during distension (15.8 +/- 0.7 versus 15.8 +/- 0.5 contractions min(-1)). The effect of balloon distension in phase IV was difficult to evaluate due to the inconsistent nature and sometimes rapidly decreasing activity in phase IV. Duodenal distension did not change frequency and amplitude of antral phase II contractions (p > 0.5). CONCLUSIONS: Duodenal balloon distension elicited ascending contractions in the canine duodenum in late phase I and in phase II. A refractory phase was demonstrated in the beginning of phase I while in phase III the frequency of contraction could not be increased further.

Animals↗

PubMed2002

Human duodenal phase III migrating motor complex activity is predominantly antegrade, as revealed by high-resolution manometry and colour pressure plots.

Abstract Late phase III migrating motor complex activity has been said to be primarily retroperistaltic but has not been assessed with high resolution manometry or three-dimensional colour pressure plots (pressure/time/distance). Duodenal phase III was examined in healthy young volunteers (seven male, two female) with a 20-lumen assembly. With the most proximal sidehole in the distal antrum, after a 4.5-cm interval 18 sideholes at 1.5-cm intervals spanned the duodenum with a final sidehole 3 cm beyond. Fasting pressures were recorded until phase III occurred. Comparisons were made between proximal (P) and distal (D) duodenum during early (E) (first 0.5-1 min) and late (L) (last 0.5-1 min) phase III. With colour pressure analysis, 121 of 180 pressure wave (PW) sequences were purely antegrade, two purely retrograde and 57 bidirectional. Ten of fifty-seven bidirectional PW sequences were complex, branching to become two separate sequences. Bidirectional sequences occurred more frequently in late than early phase III (L 43 vs. E 14 of 57), but their occurrence did not differ between proximal and distal duodenum (P31 vs. D 24 of 57). Antegrade propagation velocity was faster in late compared with early phase III (L 28.50 vs. E 17.05 mm s(-1); P = 0.006), but did not differ between proximal and distal duodenum. Colour pressure analysis also indicated an intermittent segmental pattern to phase III, with each subject exhibiting a change in velocity or direction, or a relative failure of peristalsis somewhere along the duodenum during part of phase III. Duodenal phase III is not homogenous and, in contrast with previous studies, does not primarily constitute a retroperistaltic pump. Colour pressure analysis is useful in interpreting intraluminal pressure profiles and may improve the sensitivity and specificity of clinical studies.

Adult↗