Duodenal Migrating Myoelectric Complex Research Articles

The distribution of motilin receptor in the amygdala of rats and its role in migrating myoelectric complex

Objective To investigate the distribution of the motilin receptor in the amygdala of rats and its role in regulating the duodenal migrating myoelectric complex (MMC). Methods The distribution of motilin receptor in the amygdala in adult SD rats was detected by immunohistochemistry methods, and the duodenal interdigestive MMC was recorded via the electrodes implanted in the duodenum and analyzed using a multichannel recorder. Results Motilin receptor was observed in the amygdala of rats. The great amount of motilin receptor was found in the medial amygdaloid nucleus, which was also abundant in the basolateral nucleus but less abundant in the basomedial amygdaloid nucleus, the central amygdaloid nucleus and the lateral amygdaloid nucleus. The shortening of the duodenal MMC cycle duration and the increase of the amplitude and the frequency of phase III were recorded after motilin receptors being bound with exogenous motilin in the amygdala. The effects could be completely blocked by the subdiaphragmatic vagotomy but not by the intravenous injections of atropine, phentolamine or propranolol. Anti-motilin serum could partially block these effects, and the destruction of the basolateral nucleus of the amygdala had no significant effects on the duodenal MMC. Conclusion Motilin receptor is present in all the subnuclei of the amygdala, with the greatest amount of motilin receptor present in the medial amygdaloid nucleus. Microinjections of motilin in the amygdala can shorten the duodenal MMC cycle duration and increase the amplitude and the frequency of phase III. These effects might be accomplished via the amygdala-hypothalamus-brainstem-vagus pathway, indicating the important role of the amygdala motilin receptor in the duodenal MMC regulation.

Effect of Escherichia coli heat-labile enterotoxin on the myoelectric activity of the duodenum in weaned pigs.

The objective of the present study was to elucidate the effect of subclinical doses of Escherichia coli heat-labile enterotoxin (LT) on the antro-duodenal myoelectric activities of weaned pigs. Twelve weaned pigs were surgically implanted with three pairs of electrodes on the antrum 3 cm before the pylorus, 5 and 20 cm after the pylorus on the duodenum, respectively. An infusion cannula was inserted into the duodenum between duodenal electrodes. Using a wireless telemetry recording system, an electromyography (EMG) tracing lasting at least 24 h was recorded as the control, then another 24-h EMG recording was performed with a bolus intraduodenal infusion of LT (0.1 and 0.5 microg/kg b.w.). After a 1- to 2-day break, a 5-fold higher dose of LT was administered using the same protocol. In the antrum, LT administration barely modified the EMG signal. However, in the duodenum it prolonged the duration of phase II and the migrating myoelectric complex (MMC) cycle when compared with the control. The number of duodenal MMC cycles was also significantly diminished. Moreover, the migrating velocity of phase III was increased. The migrating action potential complex (MAPC) was present both without and with LT, but occurred more frequently following LT administration. In conclusion, LT caused a dose-dependent, lagged alteration in the duodenal MMC in weaned pigs, involving a reduction of the MMC number by lengthening phase II, increased phase III migration velocity, and increased MAPC frequency. The disturbances did not, however, result in diarrhoea and may reflect the induction of a local protection mechanism of the gut to expel unwanted foreign content from the lumen of the upper gut.

Daily changes in antro-duodenal myoelectric activity in weaned pigs

AbstractThe stomach and small intestine manifest a myoelectric activity pattern called the migrating myoelectric complex (MMC), which is controlled by both environmental and intrinsic factors. The daily MMC pattern has been little investigated, therefore the purpose of the present study was to study it, in weaned pigs given food twice a day. A wireless telemetric recording system was used for 24-h electromyography of the antrum and duodenum. The activity of the antrum showed little change if any, whereas the myoelectric activity of the duodenum significantly changed with respect to the time of day and feeding in conscious pigs. Namely, there were more frequent and regular MMC cycles occurring in the duodenum at night as compared with that during daytime. This change was due to the shortening of phase II of the MMC cycles that were registered at night. Phase I of the MMC showed transient variability in relation to feeding with no impact on the day/night differences. Phase III of the duodenal MMC cycle as well as the ‘feeding pattern’ did not change along with the time of day and feeding regime. In conclusion, daily variation in the duodenum may provide different conditions for digestive processes in the day and night.

Effect of L364 718 on interdigestive pancreatic exocrine secretion and gastroduodenal motility in conscious sheep

The present study examined roles of endogenous cholecystokinin (CCK) and CCK-A receptors in the regulation of pancreatic exocrine secretion and gastroduodenal motility in conscious sheep during interdigestive period. Interdigestive exocrine secretion of ovine pancreas changed cyclically corresponding with cycle of duodenal migrating myoelectric complexes (MMC). During second phase of the duodenal MMC, intravenous injection of L364 718 at 2.45 μmol kg −1 inhibited exogenous CCK-8-induced pancreatic exocrine secretion. Intravenous infusion of the antagonist at 2.45 μmol kg −1/5 min for 5 min also inhibited significantly the pancreatic enzyme secretion without CCK-stimulation to half of that in the control, but not the fluid and bicarbonate secretion. Atropine infusion (i.v.) at 72.0 nmol kg −1/5 min significantly inhibited not only enzyme but also fluid and bicarbonate secretion. Corresponding to the inhibition of the exocrine secretion, L364 718 induced premature phase III in duodenal electromyogram (EMG) in three of the five sheep. Omasal EMG was inhibited slightly but significantly by L364 718, however, neither regular ruminal contractions nor abomasal EMG were altered by L364 718. In contrast, the atropine infusion inhibited only amplitude of ruminal contractions. These results suggest that endogenous CCK contributes to the regulation of interdigestive pancreatic exocrine secretion, omasal contractions and duodenal MMC in the ovine gastrointestinal tract via CCK-A receptors.

Intraduodenal cholecystokinin octapeptide (CCK-8) can stimulate pancreatic secretion in the calf

The effect of CCK-8 administered into the duodenal lumen and into the systemic blood on pancreatic secretion and duodenal migrating myoelectric complex (MMC) was studied in four calves. Simultaneous MMC recordings and collections of pancreatic juice were performed on valves that had been fasted overnight. Intraduodenal (0, 100, and 300 pmol/kg body wt) and intravenous (0, 30, and 100/pmol kg) infusions of CCK-8 were made for 5 min during the no spiking activity (NSA) phase of duodenal MMC associated with a nadir of periodic pancreatic secretion. CCK-8 was also administered during continuous atropine infusion (5 micrograms/kg/min). Both intraduodenal and intravenous infusions of CCK-8 resulted in marked pancreatic responses in juice outflow, bicarbonate output, and protein output. Atropine decreased pancreatic response (protein output) to intravenous CCK-8 and markedly inhibited the response (juice flow, bicarbonate, and protein output) to intraduodenal CCK-8. Infusions of CCK-8 did not affect the duration of MMC in the duodenum. Plasma CCK increased significantly after intravenous infusion, but remained unchanged after intraduodenal infusion. In conclusion, CCK-8 can stimulate pancreatic secretion from the duodenal lumen, possibly via a cholinergic mechanism in the calf.

Central administration of Tyr-MIF-1 stimulates gastrointestinal motility in rats: Evidence for the involvement of dopamine, sigma and CCK receptors

The effect of central administration of the endogenous peptide Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH 2) on the gastrointestinal myoelectric activity and its mechanism of action were studied in rats. Tyr-MIF-1 (40 & 80 μg/kg i.c.v.) stimulated antral and duodenal myoelectric activity in a multiphasic manner. On the antrum it induced a primary increase of the frequency of antral spike bursts followed by a consecutive return to control value and a second rise of the frequency. Likewise duodenal migrating myoelectric complexes (MMCs) were initially disrupted and replaced by an irregular spiking activity followed by a reaparition of the phase III of the MMCs with increased amplitude and frequency. Haloperidol (1 mg/kg i.p.) blocked all the effects of Tyr-MIF-1 whereas sulpiride (5 mg/kg s.c.) blocked only the duodenal stimulation without affecting that on the antrum. Similarly BMY-14802 (0.5 mg/kg s.c.) antagonized selectively the primary antral stimulation and the initial disruption of duodenal MMC induced by Tyr-MIF-1. L365 260 (10 μg/kg i.c.v.) has also antagonized only the initial disruption of duodenal MMCs. DTG and JO 1784 (100 μg/kg i.c.v. each) reproduced fully the effect of Tyr-MIF-1 on the duodenum but not that on the antrum. Domperidone, (+)SCH 23390, devazepide, PK 11–195 and flumazenil did not have effect on the action of Tyr-MIF-1. It is concluded that Tyr-MIF-1 stimulates the antrum involving haloperidol sensitive but non-dopamine, probably sigma receptors, and the duodenum via a pathway where central D 2 dopamine, sigma and CCK B receptors are implied.

CCK 8 neurons of the ventromedial (VMH) hypothalamus mediate the upper gut motor changes associated with feeding in rats

The effect of microinfusions of cholecystokinin octapeptide (CCK 8) and its antagonist L364,718 on duodenal and jejunal motility were evaluated by electromyography in fasted and fed rats. The rats were chronically fitted with electrodes implanted on the duodeno-jejunal wall. Steel cannulas were placed bilaterally in either the ventromedial (VMH) and lateral (LHA) hypothalamus. In 8 h fasted rats, microinfusion of CCK 8 (1 ng/kg) into the VMH disrupted the migrating myoelectric complex (MMC) and replaced it by irregular spiking activity for 45.0 ± 4.9min at the duodenal level without affecting the jejunal MMC pattern. The duration of these effects were dose-related between 1 and 50 ng/kg. When injected into the LHA at 1, 10 or 50 ng/kg, CCK 8 had no effect on either duodenal or jejunal motility. When infused bilaterally into the VHM 10 min before feeding, L364,718 (1 or 10 μg/kg) significantly reduced the duration of the postprandial disruption of MMCs by 29.1% and 35.9%, respectively, in the duodenum but not the jejunum ( P < 0.05). infused into the LHA at similar and higher dosages (1 and 10 μg/kg) L364,718 had no effect on the duration of the duodeno-jejunal fed pattern. These results suggest that, in rats, (i) CCK 8 is involved in the maintenance of the typical postprandial disruption of duodenal MMCs observed after a meal, and (ii) these effects are selectively mediated through CCK 8 receptors located in the ventromedial hypothalamic nuclei.

Involvement of Serotonergic Mechanisms in the Disruption of Ovine Duodenal Migrating Myoelectric Complex Cycles by Duodenal Acidification

Infusions of 1 and 4 mmol of HCl (pH 2.0) into the duodenal bulb of conscious sheep, within 30% of the period of the migrating myoelectric complex (MMC) cycle, induced aborally propagated premature phases of regular spiking activity (RSA) on the proximal duodenum. A transient inhibition of reticular contractions and a shortening of the period of subsequent duodenal MMC cycles were obtained with infusions of 4 mmol of HCl but not with infusions of 1 mmol. When the animals were pretreated with the 5-hydrotryptamine (5-HT) antagonists, ritanserin (0.2 mg/kg) and metergoline (0.5 mg/kg), 15 min before duodenal infusions of 4 mmol of HCl, premature RSAs and inhibition of reticular contractions were still elicited, but shortening of the subsequent duodenal MMC cycles did not occur. It is concluded that the shortening of duodenal MMC cycles induced by duodenal infusions of 4 mmol of HCl involved a serotonergic mechanism incorporating 5-HT2 receptors. The premature duodenal RSA and inhibition of reticular motility also elicited by these infusions appeared to be independent of this serotonergic system.

Biliary and pancreatic secretory component of the migrating myoelectric complex in the pig. Effect on intraduodenal pH.

The aim of the present study in the pig was to describe the biliary and pancreatic secretory component of the migrating myoelectric complex (MMC) during the interdigestive period and after feeding, and to examine the effects of the extracorporal diversion of biliary or pancreatic secretions on the MMC and on the cyclical variation of intraduodenal pH. In a first trial six pigs (50.6 +/- 1.6 kg) were fitted with a permanent catheter in the common bile duct (3 pigs) or in the pancreatic duct (3 pigs) to control the flow of these secretions. They also had a duodenal catheter to return the secretions, and antral and duodenal electrodes for simultaneous recording of motility in fasting conditions. In a second trial ten pigs (50.8 +/- 1.5 kg) underwent a similar surgical preparation (5 bile duct and 5 pancreatic duct fistulations). They had, in addition, a duodenal T-shaped cannula (19 cm distal to the pylorus) allowing continuous intraluminal pH recording parallel to the motility recording. Experiments included 4 situations: secretions returned under fed or fasted conditions; by-passed secretions in fed or fasted pigs. The flow of bile and pancreatic juice was very high during irregular spiking activity phases (ISA), peaking at the beginning of regular spiking activity phases (RSA); it was minimal during quiescent phases. The duration of the duodenal MMC and of its 3 constitutive phases was not modified by total extracorporal diversion of bile or pancreatic secretion either in the fed or fasted state. During the interdigestive period the pH was significantly reduced under bile diversion (quiescence: 6.17 vs 7.15; ISA: 4.91 vs 5.94; RSA: 5.40 vs 6.52) as well as under pancreatic juice diversion (quiescence: 5.56 vs 7.18; ISA: 4.21 vs 5.97; RSA: 5.14 vs 6.72). In fed pigs only bile diversion resulted in a small acidification during the postprandial pattern (5.07 vs 5.44) and the consecutive MMC cycles (quiescence: 5.81 vs 6.61; ISA: 4.66 vs 4.92; RSA: 5.11 vs 5.78). Nevertheless the periodicity of pH variation along the MMC cycle was unaffected in bile or pancreatic juice-deprived animals. It is concluded that a true biliary and pancreatic secretory component of MMC exists in the pig, and that these 2 secretions strongly contribute to the neutralization of the duodenal contents. However, the major determinant of the cyclical variation of the intraduodenal pH appears to be the periodicity of the acid gastric outflow.

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

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.

Contraction pattern of opossum gallbladder during fasting and after feeding.

Our major aims in this study were to determine in unanesthetized opossums the gallbladder volume, pressure, and tone during fasting as well as after feeding, model the kinetics of changes in gallbladder volume, and correlate gallbladder contractility with concurrent spike burst activity in the upper gastrointestinal tract and sphincter of Oddi (SO). In 10 animals, we implanted electrodes on the gastric antrum, duodenum, SO, and jejunum. An indwelling catheter monitored gallbladder pressure and volume. In two animals, a force transducer sutured to the gallbladder wall monitored gallbladder tone. In each animal, fasting migrating myoelectric complexes (MMCs) were recorded in the stomach and small bowel. Cyclic changes in SO spike bursts occurred in synchrony with the MMCs. During fasting, gallbladder pressure, tone, and volume showed cyclic variations. During the second half of the duodenal MMC cycle, the gallbladder exhibited phasic as well as tonic contractions associated with net gallbladder emptying, whereas during the first half of the cycle the gallbladder relaxed and refilled. Minimal gallbladder volume during the MMC cycle averaged 4.8 +/- 0.7 (SE) ml compared with a maximal volume of 7.0 +/- 0.9 ml. Decreases in gallbladder volume occurred as an exponential function, whereas increases in gallbladder were linear. After feeding, the gallbladder underwent a sustained tonic contraction, without superimposed phasic contractions. Decreases in gallbladder volume occurred exponentially to a residual volume of 2.0 +/- 0.5 ml. Net postprandial gallbladder emptying was maximal by 40 min; then the volume remained unchanged for 2-3 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of motilin on the opossum upper gastrointestinal tract and sphincter of Oddi.

We studied the effect of motilin on myoelectric activity of the sphincter of Oddi (SO) and upper gastrointestinal tract in conscious opposums. In 17 animals, bipolar electrodes were implanted on the gastric antrum, SO, duodenum, and jejunum. Subsequent 8-h recordings reconfirmed our previous findings that SO spike burst rate changed with interdigestive cycles of the gastrointestinal migrating myoelectric complex (MMC), becoming maximal during passage of phase III activity through the duodenum. In eight animals, peak motilin levels were shown to occur concurrently with maximal SO spike burst rate and MMC phase III activity in the duodenum. Motilin infusion (0.3 and 0.9 micrograms X kg-1 X h-1), given for 30-60 min starting 10 min after duodenal phase III, elicited premature MMC activity that originated in the stomach. Maximal SO activity occurred coincident with passage of premature phase III activity through the duodenum. Pulse intravenous doses of motilin (25-1,600 ng/kg) generally caused an immediate increase in spike burst activity in the gastric antrum, duodenum, and SO that lasted 3-5 min and was often followed by a premature MMC, usually starting in the antrum and progressing through the duodenum and jejunum. Increases in SO spike burst rate also occurred concurrent with motilin-induced, premature duodenal phase III. Motilin given at 5-60% of the duodenal MMC cycle length elicited premature MMCs at 10-60% of the cycle, but no premature MMCs were elicited by any of the motilin doses at the 5% intervals.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood sugar oscillations and duodenal migrating myoelectric complexes.

Blood concentration of reducing sugar and electrical activity of the duodenum were simultaneously measured in four conscious pigs, each chronically fitted with a catheter in a jugular vein, a duodenal infusion catheter, and transparietal intestinal electrodes. After a meal, blood sugar concentration exhibited cyclic variations at a frequency similar to that of the migrating myoelectric complexes (MMC) observed on the duodenum (1.6 +/- 0.3 per h). During the fasting state (15 h), glucose or xylose infusions into the duodenum also induced blood sugar oscillations at the same frequency as that of duodenal MMC (0.9 +/- 0.3 per h). Injections of xylose boluses into the duodenum induced more rapid and larger increases in blood reducing sugar concentration when injected during the last two-thirds of the phase of irregular spiking activity or during the phase of regular spiking activity than when injected during quiescence or the first third of the phase of irregular spiking activity. It is concluded that intestinal motility is a prerequisite for optimal intestinal absorption of sugar that is markedly enhanced at the time of maximal digesta flow in the pig.

Insulin and myoelectric activity of the small intestine of the pig.

The effect of insulin on the myoelectric activity of the small intestine was determined in conscious pigs. Animals were implanted with electrodes along the small intestine, a strain gage on the stomach and catheters in both saphenous arteries. Feeding modified the migrating myoelectric complex (MMC), a cyclic pattern of action potential activity of the small intestine characteristic of fasting. The first period of regular spiking activity (RSA) on the duodenum after feeding was delayed and was not followed by quiescence. Plasma insulin and glucose concentrations during the first three MMC after feeding were highest just before periods of duodenal RSA. Injection or infusion of insulin into fasted pigs with production of hypoglycemia caused disruption of stomach motility and duodenal electrical activity. The duodenal MMC was not altered when glucose to prevent hypoglycemia was infused together with insulin or when glucose was infused alone. These studies suggest that insulin is not directly responsible for the postprandial modification of MMC activity as insulin infusions only modify the MMC when hypoglycemia occurs.