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PubMed1989

Opposite central and peripheral control by endogenous opioids of intestinal motility in fed rats.

1. The effects of the inhibitors of endopeptidase EC 24.11, thiorphan and phosphoramidon administered i.c.v. (40 micrograms kg-1) i.p. (400 micrograms kg-1), or orally (400 micrograms kg-1), on intestinal motor activity in fed rats was compared to the effects of similar doses of the angiotensin converting enzyme inhibitor, captopril and the synthetic enkephalin analogue [D-Ala2 Met5] enkephalinamide (Dalamide). Drugs were administered alone or after pretreatment with naloxone or N-methyl levallorphan (300 micrograms kg-1, i.p.) given 10 min prior to gavage with a standard meal. 2. In control conditions, in the duodenum, the disruption of the migrating myoelectric complex (MMC) by gavage with a standard meal lasted between 105.6 and 119.1 min. This duration was significantly decreased by thiorphan (60.3 +/- 15.0 min), phosphoramidon (67.9 +/- 7.3 min), captopril (26.3 +/- 10.2 min) and Dalamide (42.4 +/- 9.6 min), administered i.c.v. 3. In contrast, after the i.p. administration of thiorphan, phosphoramidon and Dalamide the delay in the return of the MMC pattern was increased. Such an effect was also seen after the oral administration of phosphoramidon or Dalamide. Neither i.p. nor oral captopril administration altered the duration of postprandial pattern. 4. A prior treatment with naloxone i.p. (300 micrograms kg-1) that had no effect per se, antagonized the effect produced by i.c.v. administration of thiorphan, phosphoramidon or Dalamide, but failed to reverse the effect of captopril. In contrast, i.p. administration of N-methyl levallorphan (300pgkg-1) did not affect the response induced by central administration of thiorphan, phosphoramidon, captopril or Dalamide, but was able to prevent that of thiorphan, phosphoramidon or Dalamide when they were administered i.p. or orally. 5. These data strongly support the hypothesis of a dual control by endogenous opioids of intestinal motility in the rat: a central component that favours, and a peripheral control that delays the occurrence of the MMC profile in fed rats.

Administration, Oral↗

PubMedDate not supplied

Metoclopramide reversal of decreased gastrointestinal myoelectric and contractile activity in a model of canine postoperative ileus.

Postoperative ileus is characterized by decreased gastrointestinal myoelectric activity and motility. Metoclopramide was used to treat experimentally induced postoperative ileus in six dogs. Contractile activity was monitored by extraluminal strain gages on the pyloric antrum and proximal segment of the duodenum, and myoelectric activity was measured by recording bipolar electromyograms (EMGs) at the pyloric antrum, pyloric canal, proximal segment of the duodenum, proximal and distal parts of the jejunum, and ileum. Measurements were obtained from animals without ileus (baseline) and those with ileus that were either untreated or treated with metoclopramide. Adynamic ileus was induced by rubbing a 50 cm segment of jejunum with a dry sponge for 5 minutes and exposing the bowel to the air for 30 minutes. Treated dogs received metoclopramide (0.4 mg/kg 4 times daily [QID] intravenously [IV]), whereas untreated dogs received a saline placebo, starting 1 hour after celiotomy closure. Recordings were made for 26 hours after induction of ileus. The phases of the migrating myoelectric complex (MMC) were identified and motility index values were determined. During ileus, the MMC phase II duration was increased at the duodenum and phase III duration was decreased at the antrum, pylorus, duodenum, and proximal segment of the jejunum (p less than 0.05). Motility index values were decreased at the antrum and duodenum during ileus (p less than 0.05). Treatment with metoclopramide reversed the MMC phase III inhibition at the antrum and pylorus, and partially reversed the inhibition at the duodenum and jejunum (p less than 0.05). Motility index values were restored to preoperative baseline values with metoclopramide treatment (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Oral absorption of sodium pentobarbital and effects on gastrointestinal function.

An anaesthetic dose (40 mg/kg) of sodium pentobarbital (SP) was administered intragastrically to adult, fasted male rats at total dosing volumes of 1, 2, or 3 ml. Area under the plasma concentration-time curve did not differ for the various dosing volumes. During the initial (rapid) phase of gastric emptying all solutions containing drug appeared to empty at a faster rate than distilled water (2 ml). However, solutions containing drug emptied much more slowly than water during the terminal (slow) phase of gastric emptying. Drug solutions moved along the small intestine at approximately the same rate as distilled water. SP significantly lowered rectal temperature and slowed the propagation velocity of the migrating myoelectric complex (MMC) recorded from four serosal electrodes chronically implanted along the proximal small intestine. In addition, the drug significantly decreased the rate of MMC recurrence, extended the duration of MMC phases, and decreased slow wave frequency at all sites monitored. The results suggest that: 1) the relative oral bioavailability of sodium pentobarbital is not influenced by dosing volume within the range tested, 2) the various dosing volumes of SP tested moved through the gastrointestinal tract at an equal rate, and 3) orally administered SP significantly decreases the propagation velocity and periodicity of the MMC in the small intestine.

Administration, Oral↗

PubMed1984

Time-related effects of benzodiazepines on intestinal motility in conscious dogs.

The effects of diazepam and GABA on intestinal motility were investigated in fasted dogs fitted with strain-gauge transducers. Injected intravenously at 9.00 and 16.00 h, diazepam (0.5 mg kg-1) affected intestinal motility only during darkness i.e. from 19.00 to 7.00 h. These jejunal motor effects which were mimicked by GABA, (0.3 mg kg-1 i.v.) corresponded to a disruption of the migrating myoelectric complex (MMC) with an increased contractile activity. These results demonstrate that benzodiazepines affect the intestinal motility in dog and suggest that the effects are related to sleep-stages.

Animals↗

PubMed1989

On the relevance of non-steroidal anti-inflammatory drugs in the prevention of paralytic ileus in rodents.

In the mouse, the gastrointestinal transit of a charcoal marker, halved following the intraperitoneal administration of acetic acid, was no longer inhibited after pretreatment with the non-steroidal anti-inflammatory drugs (NSAIDs), indomethacin, ketoprofen, piroxicam or ximoprofen (0.25-2.5 mg kg-1 orally). In the fasted rat, the migrating myoelectric complex pattern of the small intestine which was disrupted for about one hour by acetic acid was unaltered by pretreatment with indomethacin or ximoprofen (0.5 mg kg-1 i.p.). In the anaesthetized rat, the inhibition by about 50% of the gastrointestinal transit due to laparotomy, did not occur following treatment with NSAIDs. It is concluded that NSAIDs prevent the occurrence of chemically-induced and postoperative ileus in rodents, an effect probably related to the analgesic properties of NSAIDs.

Animals↗

PubMed1989

Involvement of different receptors in the central and peripheral effects of histamine on intestinal motility in the rat.

The effects of histamine on intestinal motility have been investigated in conscious rats, fed or fasted, using an electromyographic method. Histamine peripherally administered (10 mg kg-1) in 15 h fasted rats induced an inhibition followed by a period of irregular spiking activity disrupting the duodenojejunal migrating myoelectric complexes (MMC) and suppressed the postprandial motor spiking activity when administered 50 min after a meal. The selective agonist of the H1-receptors, 2-pyridylethylamine (2-PEA) induced an irregular spiking activity while dimaprit acting on H2-receptors, inhibited the MMC pattern. Effects of peripherally administered histamine were antagonized by previous administration of chlorpheniramine (0.5 mg kg-1 i.p.) and in a lesser extent by cimetidine (10 mg kg-1 i.p.). Histamine (1-10 micrograms) administered intracerebroventricularly (i.c.v.) in fasted rats increased the motor cycle frequency and immediately restored the MMC pattern when given to fed rats. Among the three agonists of the H1- H2- and H3-receptors (2-PEA, dimaprit and R-alpha-methylhistamine, respectively) only R-alpha-methylhistamine (1-10 micrograms i.c.v.) was able to reproduce this effect. It is concluded that the effects of histamine on intestinal motility were centrally and peripherally mediated involving mainly H1-receptors at the peripheral level and H3-receptors at the CNS level.

Animals↗

PubMed1996

Effects of 5-hydroxytryptamine agonists on myoelectric activity of the forestomach and antroduodenal area in sheep.

To increase knowledge of the role of 5-hydroxytryptamine (5-HT) receptors in the regulation of reticuloruminal, omasal and antroduodenal myoelectric activity in sheep, the effects of 5-HT agonists on forestomach and antroduodenal myoelectric activity have been investigated in conscious sheep. 5-Carboxamidotryptamine, methysergide, alpha-methyl-5-HT, 2-methyl-5-HT, cisapride, zacopride or metoclopramide were infused intravenously for 5 min and myoelectric recordings were obtained from electrodes chronically implanted in the reticulum, rumen (dorsal sac), omasal body, abomasal antrum and duodenal bulb. The integrated activity of the reticular and ruminal spike bursts was modified only by the highest doses of alpha-methyl-5-HT, 2-methyl-5-HT, metoclopramide and cisapride. A phase III-like activity pattern was recorded in the antroduodenal area with all 5-HT-ergic agents and a dose-dependent inhibition of myoelectric activity was recorded in both reticulorumen and omasum at the same time as the antroduodenal effects. In the forestomach, methysergide alone induced inhibition of ruminal secondary contractions; 5-HT, alpha-methyl-5-HT, cisapride and metoclopramide, moreover, evoked an initial dose-dependent increase in antral activity. These results suggest that 5-HT1, 5-HT2, 5-HT3 and 5-HT4 receptors are involved in the regulation of the migrating myoelectric complex in sheep and in the genesis of forestomach hypomotility that is occasionally recorded concomitantly with the spontaneous duodenal phase III in sheep. 5-HT4 receptors also have a prokinetic action in the antral area.

Animals↗

PubMed1983

The effects of motilin on periodic myoelectric spike activity in intact and transected canine small intestine.

The effects of motilin infusions on periodic myoelectric spike activity were studied in conscious dogs with an intact small intestine and in dogs with established jejunal Thiry-Vella loops (T-V loops). Myoelectric activity was recorded from chronically implanted electrodes on the intact intestine, the anastomosed intestine and on the jejunal T-V loop. During fasting, migrating myoelectric complexes (m.m.c.s) were present in the intact and anastomosed intestine and in the T-V loop; in the latter, intervals between m.m.c.s were significantly shorter (P less than 0.05). Infusion of motilin induced premature m.m.c.s in the intact and anastomosed intestine, reducing the interval between successive m.m.c.s (P less than 0.05). In contrast, in the T-V loop, motilin significantly reduced the number of m.m.c.s (P less than 0.01) and the interval between two m.m.c.s was prolonged. After an infusion of motilin, the number of m.m.c.s in the intact and anastomosed intestine was significantly reduced (P less than 0.01), with a corresponding increase in the intervals between m.m.c.s; no further changes were observed in the T-V loop. These results demonstrate that m.m.c.s are induced by motilin in the proximal gut, suggesting a humoral mechanism for m.m.c. initiation in this region. In contrast, the genesis of m.m.c.s in jejunal T-V loops is delayed by motilin.

Action Potentials↗

PubMed1983

Electromyographic events in the stomach and small intestine of a small kangaroo, the Tammar wallaby (Macropus eugenii).

The extracellular electrical activity of the stomach and small intestine of a macropodid marsupial was studied using chronically implanted bipolar electrodes. Recordings from the elongate, tubular, haustrated stomach showed triphasic slow waves with a frequency of 5.5/min, an amplitude of 120 microV and an aborad propagation rate of 3 mm/sec. Action potentials were recorded only from the pylorus. These occurred as bursts of six to fourteen consecutive spikes. Shortly after the period of regular spike activity occurred in the adjacent duodenum action potentials in the pylorus ceased, leaving only the slow wave present for up to 20 min. Both slow waves and action potentials were recorded from the small intestine. There was no decrease in the frequency of the slow wave from the duodenum to the ileum. The slow wave frequency was 26/min on the duodenum and 25/min on the ileum. These frequencies were not affected by fasting the animals. Migrating myoelectric complex activity of the small intestine comprising three distinct electrical patterns, occurred at regular intervals. This was only slightly affected by feeding.

Action Potentials↗

PubMed1986

Small intestinal motility and transit by electromyography and radiology in the fasted and fed pig.

The pattern of small intestinal digesta transit was studied in six young pigs (20-30 kg) by simultaneous electromyography and radiology. Pigs showed migrating myoelectric complexes (m.m.c.s) in the small intestine both when fasted and after feeding. The m.m.c.s were modified by feeding; quiescence was much reduced in duration and irregular spiking activity (i.s.a.) was prolonged; m.m.c.s were not disrupted and phases of regular spiking activity (r.s.a.) were still seen after feeding. The r.s.a. phase could be recognized on the screen and in spot films from both fasting and fed pigs as a band of intense rhythmic contractions pinching off the intestine and propelling all intestinal contents ahead of it. The r.s.a. moved caudad clearing the small intestine of digesta and leaving an empty quiescent intestine behind it. It was particularly characteristic in the fasted pig where it was usually associated with the progression of a gas bubble. The pattern of m.m.c.s in both fasted and fed animals along with the intermittent nature of stomach emptying, divided digesta into batches which progressed through the small intestine. Each batch--propelled by a m.m.c.--normally took 180-190 min to pass through the small intestine. M.m.c.s had a cycle length of 70-115 min in different parts of the small intestine. Usually two or three m.m.c.s and batches of intestinal contents were present in the small intestine at any one time. 22-33% of the m.m.c.s faded out in the proximal ileum. Batches of digesta propelled by these m.m.c.s had transit times increased by one m.m.c. duration and fused with the subsequent batch. Sometimes new m.m.c.s were generated in the terminal ileum. Two patterns of transport into the large intestine were seen. Usually digesta was transported by peristaltic rushes starting 100-200 cm from the ileo-caecal junction. The rush then continued through 1-1 1/2 turns of the spiral colon; occasionally the terminal ileum emptied by slow peristalsis. In this case there was no colonic rush and digesta went into the caecum.

Action Potentials↗

PubMed2005

Synchronization of enteric neuronal firing during the murine colonic MMC.

DiI (1,1'didodecyl-3,3,3',3'-tetramethylindocarbecyanine perchlorate) retrograde labelling and intracellular electrophysiological techniques were used to investigate the mechanisms underlying the generation of spontaneously occurring colonic migrating myoelectric complexes (colonic MMCs) in mice. In isolated, intact, whole colonic preparations, simultaneous intracellular electrical recordings were made from pairs of circular muscle (CM) cells during colonic MMC activity in the presence of nifedipine (1-2 microm). During the intervals between colonic MMCs, spontaneous inhibitory junction potentials (IJPs) were always present. The amplitudes of spontaneous IJPs were highly variable (range 1-20 mV) and occurred asynchronously in the two CM cells, when separated by 1 mm in the longitudinal axis. Colonic MMCs occurred every 151 +/- 7 s in the CM and consisted of a repetitive discharge of cholinergic rapid oscillations in membrane potential (range: 1-20 mV) that were superimposed on a slow membrane depolarization (mean amplitude: 9.6 +/- 0.5 mV; half-duration: 25.9 +/- 0.7 s). During the rising (depolarizing) phase of each colonic MMC, cholinergic rapid oscillations occurred simultaneously in both CM cells, even when the two electrodes were separated by up to 15 mm along the longitudinal axis of the colon. Smaller amplitude oscillations (< 5 mV) showed poor temporal correlation between two CM cells, even at short electrode separation distances (i.e. < 1 mm in the longitudinal axis). When the two electrodes were separated by 20 mm, all cholinergic rapid oscillations and IJPs in the CM (regardless of amplitude) were rarely, if ever, coordinated in time during the colonic MMC. Cholinergic rapid oscillations were blocked by atropine (1 microm) or tetrodotoxin (1 microm). Slow waves were never recorded from any CM cells. DiI labelling showed that the maximum projection length of CM motor neurones and interneurones along the bowel was 2.8 mm and 13 mm, respectively. When recordings were made adjacent to either oral or anal cut ends of the colon, the inhibitory or excitatory phases of the colonic MMC were absent, respectively. In summary, during the colonic MMC, cholinergic rapid oscillations of similar amplitudes occur simultaneously in two CM cells separated by large distances (up to 15 mm). As this distance was found to be far greater than the projection length of any single CM motor neurone, we suggest that the generation of each discrete cholinergic rapid oscillation represents a discreet cholinergic excitatory junction potential (EJP) that involves the synaptic activation of many cholinergic motor neurones simultaneously, by synchronous firing in many myenteric interneurones. Our data also suggest that ascending excitatory and descending inhibitory nerve pathways interact and reinforce each other.

Action Potentials↗

PubMed1978

Quantitative comparison of the effects of cholecystokinin, secretin, and pentagastrin on gastrointestinal myoelectric activity in the conscious fasted dog.

The effects on gastrointestinal myoelectric activity of infused pentagastrin, cholecystokinin (CCK), and secretin at physiological doses were studied in live dogs with implanted serosal electrodes during 56 six-hour studies. Pentagastrin dose-dependently increased gastric and duodenal slow-wave frequencies; secretin and CCK did not. Pentagastrin and CCK diminished the incidence of fasting migrating myoelectric complexes (MMCs), but MMCs were abolished only in the proximal small intestine. Pentagastrin infusion was not reflected in an increased number of spikes, whereas CCK induced a dose-dependent increase in jejunal spike activity. Secretin dose-dependently decreased duodenal and jejunal spike incidence without a marked effect on MMC incidence. Analysis of patterns of spike activity showed significant dose-dependent changes with all three peptides. The different effects of pentagastrin and CCK on spike activity in these studies may have been a consequence of pentagastrin-stimulated gastric acid secretion. None of the three peptides produced a pattern of myoelectric activity which closely resembled that seen on feeding; since, unlike food, all three peptides had little or no effect on the distal small intestine, it seems unlikely that combinations of these peptides are responsible for the change induced by food. The failure of these peptides to abolish fasting patterns in the distal intestine suggests a possible mechanism for some types of post-vagotomy dysfunction.

Action Potentials↗

PubMed1987

Involvement of alpha-1 and alpha-2 adrenoceptors in the postlaparotomy intestinal motor disturbances in the rat.

The effects of phentolamine, yohimbine and prazosin on laparotomy induced intestinal motor disturbances were studied in anaesthetised fasted rats previously equipped with electrodes, chronically implanted on the duodenum and jejunum. During continuous recording of interdigestive myoelectric activity, laparotomy under thiopental anaesthesia (Nesdonal 40 mg/kg ip) induced a primary phase of total inhibition of spiking activity lasting 26.1 +/- 1.3 min (mean +/- SE) followed by a period of disorganised activity, the first propagated migrating myoelectric complex (MMC) occurring 71.4 +/- 7.9 min after laparotomy. Phentolamine (3 mg/kg), or yohimbine (1 mg/kg) given im before laparotomy decreased by 48 and 49%, respectively, the duration of postsurgical inhibition, with a normal MMC pattern occurring immediately after. In contrast, there was only a shortening of the postlaparotomy initial inhibition of spiking activity after im prazosin (100 micrograms/kg), with a late (50-60 min) recovery of the MMC pattern. These results suggest that the initial inhibition of intestinal motility induced by laparotomy may involve alpha-1 and alpha-2 adrenoceptors, while the disruption of the MMC pattern is mainly caused by the activation of alpha-2 receptors.

Adrenergic alpha-Antagonists↗

PubMed1982

Intestinal motility responses to insulin and glucagon in streptozotocin diabetic rats.

Myoelectrical and mechanical activities were chronically recorded by use of nichrome electrodes and miniaturized strain-gage transducers sutured on the serosa of the antrum, the duodenum, and the jejunum. In a first experiment (n = 6 rats) the early (0-6 h) and late (greater than 4 days) effects of streptozotocin (65 mg/kg i.v.) was recorded. In addition, the effect of insulin (1-5 IU/kg) and glucagon (6-200 micrograms/kg) administered intravenously were studied separately each in groups of seven normal and streptozotocin-induced diabetic-fed and fasted rats. The results indicated that within the 30 min following streptozotocin administration there was a significant stimulation of the duodenal and jejunal motility lasting 46 +/- 8 min. When diabetes was established as shown by the basal blood glucose level obtained in those rats (2.30 +/- 0.84 g/L), a progressive decrease of the frequency of the migrating myoelectric complex was observed along with a disorganization of the regular spiking activity phases without disturbing the basal electrical rhythm. Comparing with the basal level, a significant increase in the gastrointestinal motility indexes (MI) appeared both in fasted (p less than 0.01) and fed (p less than 0.05) normal animals, 13.1 +/- 1.6 min after an i.v. injection of 1 IU/kg insulin. Motor effects of glucagon were related to the dose. When used at 25 microgram/kg a disorganization of the spiking activity was observed with a stimulation of the contractile activity in the jejunum. At higher dosages, i.e., 100 micrograms/kg, it induced an immediate and significant decrease of motility at any level tested and lasting up to 20 +/- 7 min. The motility responses to both hormones were lower in diabetic than in normal rats.

Animals↗

PubMed1984

Relationship of electrical slow wave and spike bursts in the dog jejunum in vivo.

The temporal relationship between the slow wave and the spike bursts was studied in the fasted and the fed states in conscious dogs implanted with serosal electrodes on the jejunum. A fully automatic computerized method processed more than 225 h of recording. For each slow wave cycle that contained a spike burst, the program computed the cycle duration and the times elapsed from the beginning of the cycle to the onset and to the end of the burst. In the fasted state as well as after feeding, the spike bursts began and ended at any time within the segment of the slow wave cycle on which spike activity occurred. These results indicate that in vivo in the dog jejunum, the temporal relationship of the slow wave and spike bursts is not fixed. They suggest that the slow wave allows the spikes to occur during limited time intervals, but does not determine their precise location and duration within these intervals. Furthermore, differences existed in the patterns of the slow wave and in its relationship with spike activity (period, location, and duration of the segment on which the spike bursts occurred) between the various phases of the migrating myoelectric complex in the fasted state and the fed state.

Action Potentials↗

PubMed1988

Do motilin and pancreatic polypeptide regulate duodenal bile acid delivery?

The plasma levels of the enteric hormones, motilin and pancreatic polypeptide, cycle in association with fasting intestinal motility and are altered by feeding. Intravenous administration of motilin causes gallbladder contraction and increased sphincter of Oddi phasic motor activity, whereas pancreatic polypeptide causes gallbladder relaxation. To determine if endogenous plasma levels of motilin and pancreatic polypeptide control sphincter of Oddi and gallbladder motility, and regulate duodenal bile acid delivery, we measured during fasting and after feeding the correlation between (a) changes in plasma motilin or pancreatic polypeptide, and (b) the duodenal delivery of a steady-state hepatic output of radiolabelled bile acid. Four dogs were prepared with duodenal cannulas. Duodenal motility was recorded manometrically. Plasma levels of pancreatic polypeptide and motilin were determined during a full cycle of the migrating myoelectric complex for 20 min before and 40 min after ingestion of a standard meal. To assess the effect of the sphincter of Oddi and the gallbladder together, or the gallbladder alone on duodenal bile acid delivery, the dogs received a continuous i.v. infusion of [14C]taurocholic acid (TCA); duodenal delivery of TCA was quantitated with the sphincter of Oddi intact using duodenal marker perfusion, or with the sphincter of Oddi cannulated and zero outflow resistance. In the interdigestive period with the sphincter of Oddi intact, only 0.1 (r2) of the variance of duodenal bile acid delivery can be predicted from the variance of motilin, and the correlation of plasma pancreatic polypeptide with duodenal TCA delivery is opposite that expected if pancreatic polypeptide caused gallbladder relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Intestinal motility during acute Yersinia enterocolitica enteritis in rabbits.

To determine if Yersinia enterocolitica (YE) enteritis is associated with an alteration of intestinal myoelectric and motor activity, and with an increased rate of aboral transit, New Zealand white rabbits (500-900 g) were surgically prepared with ileal bipolar electrodes and a manometry catheter adjacent to the distal electrode. One week later animals were inoculated with 10(10) organisms of YE in 10 mL NaHCO3 (infected group) or 10 mL NaHCO3 (sham-infected pair-fed and control groups). Daily food intake, weight gain, YE excretion, and stool pattern were noted. Intestinal myoelectric and motor activity over a 6- to 8-h period before and 3, 6, and 14 days after inoculation was compared in infected (I), pair-fed (PF), and control (C) groups. Intestinal transit was evaluated in I and C animals on days 3 and 6 after inoculation by measuring the distribution in the intestinal lumen of 51Cr 20 min after it was instilled directly into the jejunum. Infected animals exhibited diarrhea, fecal excretion of YE, and significantly decreased food intake, weight gain, and survival (11.4 +/- 0.6 days). Infection was associated with a significant (p less than 0.05) decrease in both the cycle period of the migrating myoelectric complex (MMC) and the total number of single, paired, and (or) clustered contractions per MMC, and a significant (p less than 0.001) increase in duration of phase III of the MMC. There was no change in intestinal slow wave frequency (19 cycles/min), motility index per MMC, or the percentage of contractions that propagated in an orad (7%) or aboral (69%) direction or that appeared stationary (25%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1983

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)

Ampulla of Vater↗