Relationship of postprandial motilin, gastrin, and pancreatic polypeptide release to intestinal motility during vagal interruption

1992 ◽  
Vol 70 (8) ◽  
pp. 1148-1153 ◽  
Author(s):  
S. A. Chung ◽  
G. R. Greenberg ◽  
N. E. Diamant
Keyword(s):  
Pancreatic Polypeptide ◽  
Intestinal Motility ◽  
Plasma Concentrations ◽  
Phase Iii ◽  
Fed State ◽  
Vagal Blockade ◽  
Small Intestinal ◽  
Relationship Of ◽  
Vagal Cooling ◽  
Sustained Increase

Experiments were performed to determine how postprandial motilin, gastrin, and pancreatic polypeptide plasma concentrations measured during vagal blockade relate to coincident small intestinal motility patterns. Feeding produced a postprandial pattern of intestinal motility coincident with a sustained increase in gastrin and pancreatic polypeptide and a decline in motilin plasma concentrations. Vagal blockade replaced the fed pattern with one similar to migrating motor complex (MMC) activity. Highest motilin plasma concentrations were observed during phase III of this MMC-like activity, as occurs in the fasted state. Vagal blockade reduced but did not abolish the postprandial increase in plasma gastrin and pancreatic polypeptide concentrations. Termination of vagal cooling produced a decline in motilin and an elevation in gastrin and pancreatic polypeptide concentrations, coincident with the return of the fed pattern. In conclusion, during vagal blockade in the fed state (i) motilin, but not gastrin or pancreatic polypeptide plasma concentrations, fluctuate with the MMC-like activity, and any measurement of motilin concentrations under these circumstances must be interpreted on the basis of gut motility patterns, and (ii) gastrin and pancreatic polypeptide concentrations are marginally elevated, but these changes are not enough to disrupt the MMC or have any motor effect. Lastly, the fed pattern and the postprandial changes in motilin, gastrin, and pancreatic polypeptide concentrations are in part dependent upon intact vagal pathways.Key words: gastrointestinal motility, vagus, motilin, gastrin, pancreatic polypeptide.

Small intestinal motility in fasted and postprandial states: effect of transient vagosympathetic blockade

1987 ◽  
Vol 252 (3) ◽  
pp. G301-G308 ◽  
Author(s):  
S. A. Chung ◽  
N. E. Diamant
Keyword(s):  
Small Bowel ◽  
Intestinal Motility ◽  
Gastric Fundus ◽  
Phase Iii ◽  
Entire Small Bowel ◽  
Vagal Blockade ◽  
Small Intestinal Motility ◽  
Proximal Small Bowel ◽  
Small Intestinal ◽  
Gastric Contractions

We investigated vagal control of the migrating myoelectric complex (MMC) and postprandial pattern of the canine small intestine. Gastric and small intestinal motility were monitored in six conscious dogs. The vagosympathetic nerves, previously isolated in bilateral skin loops, were blocked by cooling. To feed, a meat-based liquid food was infused by tube into the gastric fundus. MMC phases I, II, III, and IV were observed in the fasted state. On feeding, the fed pattern appeared quickly in the proximal small bowel but was delayed distally. Vagal blockade abolished all gastric contractions and spiking activity as well as the small bowel fed pattern. During vagal blockade, the small bowel exhibited MMC-like migrating bursts of spikes in both the fasted and fed states. The migration and cycling of these bursts were not significantly different from the MMC, but the duodenal and jejunal phase II was absent or shortened. On termination of vagal blockade, normal fasting or fed activity reappeared but with a delay in the fed pattern distally. We conclude: the ileum is the least sensitive to vagal blockade; the fasting vagal influence is exerted primarily on phases I and II of the duodenal and jejunal MMC; the fed pattern throughout the entire small bowel is normally dependent upon vagal integrity; the phase III-like bursts of activity seen during vagal blockade likely represents the intrinsic small bowel MMC, which is vagally independent.

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

1985 ◽  
Vol 63 (12) ◽  
pp. 1495-1500 ◽  
Author(s):  
P. Poitras ◽  
M. Lemoyne ◽  
D. Tasse ◽  
L. Trudel ◽  
T. Y. Yamda ◽  
...  
Keyword(s):  
Pancreatic Polypeptide ◽  
Plasma Levels ◽  
Intestinal Motility ◽  
Plasma Concentrations ◽  
Statistical Correlation ◽  
Significant Rise ◽  
Phase Iii ◽  
Blood Levels ◽  
Plasma Motilin ◽  
Related Increase

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

scholarly journals Evidence that nitric oxide mechanisms regulate small intestinal motility in humans

Gut ◽  
1999 ◽  
Vol 44 (1) ◽  
pp. 72-76 ◽  
Author(s):  
A Russo ◽  
R Fraser ◽  
K Adachi ◽  
M Horowitz ◽  
G Boeckxstaens
Keyword(s):  
Motor Activity ◽  
Intestinal Motility ◽  
Random Order ◽  
Neural Mechanisms ◽  
Phase Iii ◽  
First Episode ◽  
Small Intestinal Motility ◽  
Small Intestinal ◽  
Synthase Inhibitor

BackgroundNon-cholinergic non-adrenergic neural mechanisms involving nerves containing NO have been shown to modulate smooth muscle in the gastrointestinal tract, and it has been suggested that release from tonic NO inhibition may be important in the regulation of cyclical fasting small intestinal motility.AimsTo evaluate the role of NO mechanisms in the regulation of fasting small intestinal motor activity in humans using a specific NO synthase inhibitor,NG-monomethyl-l-arginine ( l-NMMA).MethodsIn seven healthy male volunteers, duodenal and jejunal pressures were measured for four hours with a nine lumen manometric catheter. Volunteers attended on four separate days on which they received an intravenous infusion of either saline or l-NMMA (0.5, 2, or 4 mg/kg/h) in random order. Intravenous infusions began 10 minutes after completion of phase III of the migrating motor complex (MMC).ResultsThe first episode of phase III activity occurred earlier after infusion of 2 and 4 mg/kg/h l-NMMA than after infusion of 0.5 mg/kg/hl-NMMA or saline (mean (95% confidence interval) 52 (36–68) and 57 (18–97) v 116 (69–193) and 145 (64–226) minutes respectively) with a resultant MMC cycle length of 82 (59–105) and 86 (46–126) v 132 (49–198) and 169 (98–240) minutes respectively. The total number of phase III activities during the four hour recording was increased (p<0.05) by l-NMMA at a dose of 4 mg/kg/h (2 (1–3)) but not at 2 mg/kg/h (1.5 (1–2)) or 0.5 mg/kg/h (1.3 (1–2)) compared with saline (1.3 (0.6–2)). l-NMMA had no effect on the duration, velocity, number of contractions per minute, length of migration, or site of origin of phase III of the MMC. The duration of phase I activity was shorter (p<0.05) with 4 mg/kg/hl-NMMA than with saline (12 (1–23)v 31 (19–44) minutes).ConclusionsThese observations suggest that NO mechanisms play a role in the regulation of fasting small intestinal motor activity in humans.

Vagal control of migrating motor complex-related peaks in canine plasma motilin, pancreatic polypeptide, and gastrin

1983 ◽  
Vol 61 (11) ◽  
pp. 1289-1298 ◽  
Author(s):  
K. E. Hall ◽  
G. R. Greenberg ◽  
T. Y. El-Sharkawy ◽  
N. E. Diamant
Keyword(s):  
Pancreatic Polypeptide ◽  
Time Course ◽  
Late Phase ◽  
Migrating Motor Complex ◽  
Phase Iii ◽  
Motor Complex ◽  
Vagal Blockade ◽  
Excitatory Pathways ◽  
Plasma Motilin ◽  
Canine Plasma

The role of the vagus nerve in the control of fasting plasma pancreatic polypeptide (PP), gastrin, and motilin levels was investigated in conscious dogs. Lowest plasma levels of motilin (81 ± 8 pmol/L), PP (19 ± 1 pmol/L) and gastrin (5 ± 1 pmol/L) were observed during phase I of the migrating motor complex (MMC). Significant peaks in plasma motilin (127 ± 11 pmol/L, P < 0.005), PP (26 ± 2 pmol/L, P < 0.005), and gastrin (14 ± 2 pmol/L, P < 0.005) were seen, coinciding with the appearance of phase II (PP and gastrin) or phase III (motilin) of the migrating motor complex in the upper gut. Whereas bilateral vagal blockade abolished the peaks in PP and gastrin, a significant (P < 0.025) increment in plasma motilin remained, which correlated with the late phase III equivalent of the vagally independent complex (VIC) in the duodenum. This VIC-related motilin peak (170 ± 20 pmol/L) was significantly higher (P < 0.025) and the time course (9 ± 2 min) significantly shorter (P < 0.01) than the peak (127 ± 11 pmol/L) and duration (31 ± 9 min) observed without vagal blockade. Thus, in fasting, the cyclical increments of PP and gastrin are both dependent on excitatory vagal innervation, whereas excitatory pathways controlling phase III associated peak motilin release are nonvagal. In addition, the pattern of fasting motilin release and the amplitude of peak motilin secretion may be affected by vagal inhibition.

Circadian coupling between pancreatic secretion and intestinal motility in humans

2001 ◽  
Vol 280 (2) ◽  
pp. G273-G278 ◽  
Author(s):  
Jutta Keller ◽  
Gabriele Gröger ◽  
Leelamma Cherian ◽  
Britt Günther ◽  
Peter Layer
Keyword(s):  
Pancreatic Polypeptide ◽  
Pancreatic Secretion ◽  
Intestinal Motility ◽  
Plasma Concentrations ◽  
Pancreatic Enzyme ◽  
Secretory Activity ◽  
Exocrine Secretion ◽  
Motility Index ◽  
Cholinergic Tone ◽  
Pancreatic Exocrine

Human interdigestive intestinal motility follows a circadian rhythm with reduced nocturnal activity, but circadian pancreatic exocrine secretion is unknown. To determine whether circadian changes in interdigestive pancreatic secretion occur and are associated with motor events, pancreatic enzyme outputs, proximal jejunal motility, and plasma pancreatic polypeptide concentrations were measured during consecutive daytime and nighttime periods (12 h each) in seven healthy volunteers using orojejunal multilumen intubation. Studies were randomly started in the morning or evening. Nocturnally, motility decreased (motor quiescence: 67 ± 22 vs. 146 ± 37 min; motility index: 3.59 ± 0.33 vs. 2.78 ± 0.40 mmHg/min; both P < 0.05) but amylase output increased (273 ± 78 vs. 384 ± 100 U/min; P < 0.05) and protease output remained unchanged ( P > 0.05); consequently, enzyme/motility ratio increased. Amylase outputs were always lowest during phase I. Motor but not pancreatic circadian activities were associated with sleep. Pancreatic polypeptide plasma concentrations were unchanged. Consequently, intestinal motor and pancreatic exocrine functions may have different circadian rhythms, i.e., decreased motor and stable secretory activity during the night. However, the association between individual phases of interdigestive motor and secretory activity is preserved. The nocturnal increase in enzyme/motility ratio is probably not caused by increased cholinergic tone.

Concentration-Dependent Stimulation of Intestinal Phase III of Migrating Motor Complex by Circulating Serotonin in Humans

1998 ◽  
Vol 94 (6) ◽  
pp. 663-670 ◽  
Author(s):  
Mikael Lördal ◽  
Håkan Wallén ◽  
Paul Hjemdahl ◽  
Olof Beck ◽  
Per M. Hellström
Keyword(s):  
Small Intestine ◽  
Intestinal Motility ◽  
Low Dose ◽  
Migrating Motor Complex ◽  
Phase Iii ◽  
Motility Index ◽  
Motor Complex ◽  
Small Intestinal Motility ◽  
Respiratory Parameters ◽  
Small Intestinal

1. The influence of circulating 5-hydroxytryptamine (serotonin) on small intestinal motility was investigated in healthy volunteers. 2. Small intestinal motility was studied by means of a constantly perfused multi-channel manometry tube, connected to a computer system. 3. Intravenous infusions of either 5-hydroxytryptamine at increasing doses or saline were given over a period of 4 h. 4. 5-Hydroxytryptamine infusion dose-dependently increased plasma 5-hydroxytryptamine from approximately 2 to 10 and 25 nmol/l respectively, as well as urinary excretions of 5-hydroxytryptamine and 5-hydroxyindole acetic acid, a major 5-hydroxytryptamine metabolite. 5. The number of phase III of the migrating motor complex originating in the small intestine was dose-dependently increased by 5-hydroxytryptamine, and found to correlate to the plasma concentration of 5-hydroxytryptamine. The fraction of phase III also increased at the expense of phase II activity. In addition, 5-hydroxytryptamine increased the motility index, propagation velocity of phase III activity and the amplitude of contractions during phase III. 6. Whereas the low dose of 5-hydroxytryptamine (15 nmol · min−1 · kg−1) had no haemodynamic effects, an increase in heart rate by approximately 20 beats/min, without change in blood pressure, was observed at the higher dose (60 nmol · min−1 · kg−1). Respiratory parameters did not change during infusion of 5-hydroxytryptamine at either dose. 7. In conclusion, elevation of circulating 5-hydroxytryptamine by intravenous infusion results in more frequent and faster propagating migrating motor complexes in the human small intestine during the interdigestive period.

Pancreatic polypeptide (PP) and migrating motor complexes (MMC) in the dog: Effect of vagal blockade

1980 ◽  
Vol 1 ◽  
pp. S44 ◽  
Author(s):  
GR Greenberg ◽  
KE Hall ◽  
H Mui ◽  
TY El-Sharkawy ◽  
NE Diamant
Keyword(s):  
Pancreatic Polypeptide ◽  
Vagal Blockade

scholarly journals Evaluation of Small Intestinal Motility in a Rat Model of Irritable Bowel Syndrome

2021 ◽  
Author(s):  
Masamichi Sato ◽  
Takahiro Kudo ◽  
Nobuyasu Arai ◽  
Reiko Kyodo ◽  
Kenji Hosoi ◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Small Intestine ◽  
Real Time ◽  
Rat Model ◽  
Intestinal Motility ◽  
Restraint Stress ◽  
Rat Models ◽  
Small Intestinal Motility ◽  
Small Intestinal ◽  
Irritable Bowel

Abstract Background: The correlation between small intestinal motility alteration and irritable bowel syndrome (IBS) is not well evaluated. Aims: To assess the small intestinal and colonic transits in an IBS rat model with restraint stress and determine the role of small intestinal motility in the IBS pathophysiology.Methods: Restraint stress was utilized to make adolescent IBS rat models that were evaluated for clinical symptoms, including stool frequency and diarrhea. The small intestinal motility and transit rate were also evaluated. The amounts of mRNA encoding corticotropin-releasing hormone, mast cell, and serotonin (5-Hydroxytryptamine; 5-HT) receptor 3a were quantified using real-time polymerase chain reaction (PCR); the 5-HT expression was evaluated using immunostaining.Results: Restraint stress significantly increased the number of fecal pellet outputs, stool water content, and small intestinal motility in the IBS rat models. There was no difference in real-time PCR results, but immunostaining analysis revealed that 5-HT expression in the small intestine was significantly increased in the IBS rat models.Conclusions: In the adolescent rat model of IBS with restraint stress, we observed an increase in small intestinal and colonic motility. In the small intestine, enhanced 5-HT secretion in the distal portion may be involved in increasing the small intestinal motility.

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