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At least 19 recordsLinked to original sources
PubMed1983

Enteric mechanisms of initiation of migrating myoelectric complexes in dogs.

The enteric mechanisms governing initiation of migrating myoelectric complexes were studied in 6 conscious dogs, each implanted with a set of 12 bipolar electrodes on the small intestine. The small intestine was transected and reanastomosed at three sites to give four isolated segments of equal length. Each segment had three implanted electrodes. All four isolated segments generated migrating myoelectric complexes which were, initially, totally independent of each other in time. The most proximal segment had the longest mean migrating myoelectric complex time period (106.2 +/- 10.1 SEM min) and the second segment had the shortest mean migrating myoelectric complex time period (66.8 +/- 6.7 SEM min). Distal to the second segment, the mean migrating myoelectric complex time period increased progressively (83.1 +/- 11.2 SEM min and 95.8 +/- 7.6 SEM min, respectively). Isolation of the small intestine into segments did not significantly change migrating myoelectric complex propagation characteristics such as velocity and direction of propagation within each segment. The mean duration of phase 3 activity was not affected in the first segment but increased significantly in the distal three segments (p less than 0.05). The propagation of migrating myoelectric complexes across the sites of transection and reanastomosis started recovering 45-60 days after surgery and recovered fully by 98-108 days. The study findings show that enteric mechanisms control the initiation of migrating myoelectric complexes. Each small segment of the small intestine is capable of initiating migrating myoelectric complexes of its own and behaves as a relaxation oscillator. In the intact small intestine, regional migrating myoelectric complex oscillators are coupled by the intrinsic neurons so that the proximal oscillators drive the distal oscillators. Recovery of migrating myoelectric complex propagation across sites of transection and reanastomosis suggest that intrinsic nerves regenerate after transection.

Action Potentials↗
PubMed1997

Evidence for the involvement of 5-HT4 receptors in the 5-hydroxytryptamine-induced pattern of migrating myoelectric complex in sheep.

1. The effects induced by 5-hydroxytryptamine (5-HT) on gastrointestinal myoelectric activity in conscious sheep were recorded through electrodes chronically implanted and analysed by computer. The 5-HT receptors and the cholinergic neuronal pathways involved in these actions were investigated. 2. The intravenous (i.v.) administration of 5-HT (2, 4 and 8 micrograms kg-1 min-1, 5 min) induced an antral inhibition concomitant with a duodenal activity front that migrated to the jejunum, followed by a period of intestinal inactivity. This myoelectric pattern closely resembled that observed in the phases III and I of the migrating myoelectric complex (MMC) in sheep. The 0.5 microgram kg-1 min-1 dose evoked the same pattern in only two out of the six animals used. Likewise, the 1 microgram kg-1 min-1 dose similarly affected four of the six animals. In addition, a transient stimulation was observed in the antrum and jejunum when the two highest doses were used. 3. The 5-HT1 antagonist, methiothepin (0.1 mg kg-1), the 5-HT2 antagonists, ritanserin (0.1 mg kg-1) and ketanserin (0.3 mg kg-1), the 5-HT3 antagonists, granisetron (0.2 mg kg-1) and ondansetron (0.5 mg kg-1), as well as the 5-HT4 antagonist, GR113808 (0.2 mg kg-1), did not modify the spontaneous gastrointestinal myoelectric activity. However, the cholinoceptor antagonists, atropine (0.2 mg kg-1) and hexamethonium (2 mg kg-1), inhibited gastrointestinal activity. 4. When these antagonists were injected i.v. 10 min before 5-HT (2 or 4 micrograms kg-1 min-1, 5 min), only GR113808, atropine and hexamethonium were able to modify the 5-HT-induced actions, all of them being completely blocked by the three antagonists. 5. Our data show that 5-HT initiates a MMC-like pattern in the gastrointestinal area in sheep through 5-HT4 receptors. Furthermore, these actions are mediated by cholinergic neural pathways involving muscarinic and nicotinic receptors. However, our results do not indicate a role for either 5-HT1, 5-HT2 or 5-HT3 receptors in the 5-HT-induced effects.

Animals↗
PubMed1997

Kinetics of pancreatic juice secretion in relation to duodenal migrating myoelectric complex in preruminant and ruminant calves fed twice daily.

Daily secretion of pancreatic juice, including postprandial responses to food, was investigated in two groups of calves: preruminant (fed with liquid food) and ruminant (fed with solid food). Male Friesian calves (1 week old and 6 weeks old) were surgically fitted with a pancreatic duct catheter, duodenal cannula and two duodenal electrodes. Continuous 24 h collections of pancreatic juice and myoelectrical recordings were performed with minimal restraint and disturbance of animals. In both groups of calves clear periodic fluctuations in pancreatic juice secretion (volume, protein output and trypsin activity) coinciding with duodenal migrating myoelectric complexes (MMC) were recorded. Secretion of juice per cycle and per day was greater in ruminant calves, but the frequency and amplitude of cycles were lower in this group. There were no differences between day and night-time preprandial pancreatic cycles and duodenal MMC in preruminant calves, whilst in ruminant calves, evening MMC were longer than morning MMC. The pancreatic cephalic phase (increase of volume flow, protein output and trypsin activity during and just after food intake) was significant only in preruminant calves following morning feeding. Postprandial pancreatic cycles did not differ from preprandial cycles, except the pancreatic cycle (juice volume and trypsin activity) in which food was offered in preruminant calves. No gastric or intestinal phase was observed in either group of calves. In conclusion, biological cycles of the gastrointestinal tract are present in both preruminant and ruminant calves, and these cycles evolve along with the change from liquid to solid food.

Animals↗
PubMed2003

Physiological regulation and NO-dependent inhibition of migrating myoelectric complex in the rat small bowel by OXA.

Orexin A (OXA)-positive neurons are found in the lateral hypothalamic area and the enteric nervous system. The aim of this study was to investigate the mechanism of OXA action on small bowel motility. Electrodes were implanted in the serosa of the rat small intestine for recordings of myoelectric activity during infusion of saline or OXA in naive rats, vagotomized rats, rats pretreated with guanethidine (3 mg/kg) or N(omega)-nitro-L-arginine (L-NNA; 1 mg/kg). Naive rats were given a bolus of the orexin receptor-1 (OX1R) antagonist (SB-334867-A; 10 mg/kg), and the effect of both OXA and SB-334867-A on fasting motility was studied. Double-label immunocytochemistry with primary antibodies against OXA, neuronal nitric oxide synthase (nNOS), and OX1R was performed. OXA induced a dose-dependent prolongation of the cycle length of the migrating myoelectric complex (MMC) and, in the higher doses, replaced the activity fronts with an irregular spiking pattern. Vagotomy or pretreatment with guanethidine failed to prevent the response to OXA. The OXA-induced effect on the MMC cycle length was completely inhibited by pretreatment with L-NNA (P < 0.05), as did SB-334867-A. The OX1R antagonist shortened the MMC cycle length from 14.1 (12.0-23.5) to 11.0 (9.5-14.7) min (P < 0.05) during control and treatment periods, respectively. Colocalization of OXA and nNOS was observed in myenteric neurons of the duodenum and nerve fibers in the circular muscle. Our results indicate that OXA inhibition of the MMC involves the OX1R and that activation of a L-arginine/NO pathway possibly originating from OX1R/nNOS-containing neurons in the myenteric plexus may mediate this effect. Endogenous OXA may have a physiological role in regulating the MMC.

Animals↗
PubMed1996

Luteinizing hormone and human chorionic gonadotropin fragment the migrating myoelectric complex in rat small intestine.

We hypothesized that sex hormones may affect motility disorders because these diseases occur more often in women than in men, and symptoms often occur or worsen after ovulation. Luteinizing hormone (LH) is predominantly secreted by the anterior pituitary midway through the menstrual cycle; it results in the development of the corpus luteum. LH levels also increase after bilateral gonadectomy. LH and human chorionic gonadotropin (hCG) bind to the same receptor, but rats lack hCG. To assess how LH and hCG influence myoelectric activity of the small intestine and to test the specificity of the LH receptor, we implanted electrodes on the jejunum of female rats. LH (0.1 or 0.5 NIH units) was administered intraperitoneally to intact and gonadectomized rats and 0.5 NIH units to rats that had been both hypophysectomized and gonadectomized; intact animals were treated with 100 units USP of hCG. Recordings were made with the rats in fasted and in fed states, and their intestinal motility was analysed. The most striking effects of LH, hypophysectomy, and hCG were the same: phase III of the migrating myoelectric complex was markedly fragmented and its duration lengthened (P < 0.0001). Gonadectomy alone and gonadectomy with hypophysectomy also increased fragmentation and phase III duration (P < 0.01 or better). LH receptors respond similarly to LH and hCG, and both hormones alter myoelectric activity of the rat small intestine in comparable ways.

Animals↗
PubMed1996

[Effect of jiawei sijunzi decoction on migrating myoelectric complex in 8 Gy irradiated rats].

The normal intestinal migrating myoelectric complex (MMC) of rats recorded by implanted electrode consists of four phases (phase I, II, III and IV). After 8 Gy of gamma-radiation for 1 hour to 7 days, the MMC cycle in most of the rats were disappeared only phase I or II existed with minute's rhythm. 1 hour or 3 days after radiation, the MMC cycle appeared in a few rats with the phase II shortened significantly (P < 0.05). Results of observation on effect of Jiawei Sijunzi Decoction on MMC after radiation showed the changed phase and cycle of MMC were normalized basically by the medication. These results suggested that the Jiawei Sijunzi decoction could improve the intestinal disturbances caused by radiation, it might be one of the reason of its alleviating effect on the radiation diarrhea.

Animals↗
PubMed1989

Migrating myoelectric complex demonstrated in four avian species.

The migrating myoelectric complex (MMC) is demonstrated in four avian species: three gallinaceous birds (Gallus, Phasianus, Coturnix) and an owl (Strix). The complex in birds is strikingly similar to the MMC that is known in mammalian species. It has the same basic pattern of quiescence, followed by a period of irregular spike activity, then a period of intense regular spike activity, and finally a return to quiescence. The frequency and duration of avian MMCs are similar to those of mammals, but the propagation velocity and slow-wave frequency are slower. Granivorous birds (Gallus, Phasianus) and carnivores (Strix) exhibit the same basic motility patterns whether in the fed or fasted states. Interspecific differences occur, however, in the details of frequency, propagation velocity, duration, and slow-wave frequency. The closely related galliforms (chickens, pheasants) are more similar to each other in MMC characteristics than either is to the more distantly related owls.

Action Potentials↗
PubMed1988

Local nerve blockade by tetrodotoxin induces ectopic phase 3 of the migrating myoelectric complex in dogs.

The effect on the migrating myoelectric complex (MMC) of local nerve blockade in the jejunum was studied in five unanesthetized dogs. A silastic catheter was implanted in a terminal branch of a jejunal artery, perfusing a 5- to 10-cm segment, 45 cm below the ligament of Treitz. Small-bowel motor activity was studied electromyographically with implanted electrodes. Three different doses of tetrodotoxin (166, 333, 500 ng/kg/h) were administered intra-arterially for 5 h. During the 333- and 500-ng but not during the 166-ng/kg/h perfusions ectopic activity fronts started just below the perfused segment. At this time no phase-3 activity was observed in the proximal bowel. In addition to ectopic fronts normal MMCs were observed during the perfusions. These observations show that local nerve blockade induces phase-3 activity, probably by inhibiting an inhibitory nerve action.

Animals↗
PubMed1984

Morphine-initiated migrating myoelectric complexes in the fed state in dogs.

The ingestion of a meal in nonruminants disrupts the cycling of migrating myoelectric complexes for several hours. We investigated the initiation of phase III activity during the postprandial state by morphine. Small intestinal recordings were made from 5 dogs by surgically implanted electrodes. Morphine boluses (5-400 micrograms/kg) were given during the fasted state and after a meal. Morphine initiated premature phase III activity in the fasted state and it also initiated phase III activity in the postprandial state. Motilin did not initiate phase III activity in the postprandial state. The mean durations of morphine-initiated phase III activity in the fasted state and in the postprandial state were not significantly different from that of spontaneous phase III activity; however, morphine-initiated phase III activity in both the fasted and fed states migrated faster than spontaneous phase III activity in the proximal half of small intestine but not in the distal half. The latent period for the initiation of phase III activity was significantly greater 20-40 min after the meal than 2 h after the meal. The minimum dose of morphine required to initiate phase III activity in the fed state decreased progressively after the initial increase until it reached fasted levels 7-10 h after the meal. Spontaneous phase III activity appeared after this period. We conclude that (a) morphine temporarily overcomes the disruption of migrating myoelectric complex cycling after a meal; (b) morphine acts at different sites than motilin to initiate phase III activity; (c) the increased refractoriness of migrating myoelectric complex cycling mechanisms after a meal may play a role in the disruption of migrating myoelectric complex cycling.

Animals↗
PubMed1982

Effects of motilin, somatostatin, and pancreatic polypeptide on the migrating myoelectric complex in pig and dog.

Spiking activity of the gastrointestinal tract was recorded in 4 fasted pigs and 4 fasted dogs during the intravenous infusion at two rates, 5 (rate A) and 20 (rate B) ng . kg-1 . min-1 of 13-Nle-motilin, somatostatin, and bovine pancreatic polypeptide. Infusions continued for 2 h in pigs and for 5 h in dogs. 13-Nle-Motilin was unable to induce a migrating myoelectric complex or to modify its frequency in the pig at either rate of infusion. In contrast, the infusion of 13-Nle-motilin at rate B in the dog induced a migrating myoelectric complex but delayed the occurrence of the following migrating myoelectric complex. However, the mean duration (74 +/- 22 min) of the migrating myoelectric complex interval in the 5 h of infusion did not significantly change compared with the control period (92 +/- 8 min). At rate B, somatostatin inhibited the gastroduodenal spiking activity in the pig and disrupted the migrating myoelectric complex pattern, whereas this hormone at both rates of infusion increased the frequency of the migrating myoelectric complex by 69.3% and 17.2%, respectively, in the dog. The infusion of bovine pancreatic polypeptide increased the frequency of the migrating myoelectric complex significantly by 36.4% and 82% at rates A and B in the pig and by 148% at rate A in the dog. Bovine pancreatic polypeptide also inhibited spiking activity in the duodenum but not in the jejunum at rate B in the dog. These results suggest that pancreatic polypeptide, but not somatostatin, may have a regulatory function on the rhythmicity of the migrating myoelectric complex in the dog and pig and that motilin does not control the occurrence of duodenal migrating myoelectric complex in the pig.

Action Potentials↗
PubMed1990

Human migrating myoelectric complex in relation to gastrointestinal transit of a meal.

Feeding interrupts the migrating myoelectric complex in most mammals. This study aimed to assess whether resumption of the migrating myoelectric complex in the human duodenum after eating was related to the gastrointestinal transit of the meal. Five healthy subjects participated in the study. After eating a radiolabelled test meal consisting of mixed liquid and solids, duodenal myoelectric activity and gastrointestinal transit of the meal were determined simultaneously. In spite of considerable variation in entire gastric emptying time between subjects (range 2.5-5.0 hours), significant correlation was found between the completion of gastric emptying and the resumption of duodenal phase III activity within subjects (p less than 0.01). A new technique for recording the duodenal myoelectric activity was used.

Adult↗
PubMed1993

Intestinal migrating myoelectric complexes in rats with acute pancreatitis and bile duct ligation.

Intestinal migrating myoelectric complexes (MMC) were studied in rats subjected to common bile duct ligation. Four pairs of bipolar electrodes were implanted on the jejunum and the ileum of 21 rats. Animals were allowed to recover 7 days before electrical recordings were made. Bile duct ligation at the entrance to the duodenum (low) or above the pancreas (high) or sham operation was performed. MMCs were recorded before and 48 and 72 hr after the operation in each animal. MMC intervals were unchanged following high ligation or sham operation. However, 48 hr after low bile duct ligation, the MMC interval (20.6 +/- 2.5 min) was significantly prolonged compared with that before ligation (14.0 +/- 1.2 min). Further prolonged intervals (28.4 +/- 4.2 min) were observed 72 hr after the ligation. There were no significant differences among the slow wave frequencies in any group of animals, being in the range of 34.1 +/- 1.1 to 36.3 +/- 1.0 cycles/min. Thus, the MMC pattern in this rat model may be affected by the development of acute pancreatitis. The mechanism(s) responsible for altering the MMC pattern are not known; however, hepatic biliary secretion alone does not appear to play a primary role.

Acute Disease↗
PubMed1989

Role of muscarinic receptor subtypes in the regulation of migrating myoelectric complex in the dog.

The role played by muscarinic receptor subtypes in the regulation of the migrating myoelectric complex was investigated in 7 dogs chronically implanted with bipolar electrodes along the small intestine. Pirenzepine (3-300 micrograms/kg i.v.) and atropine (1-30 micrograms/kg i.v.) were used as selective and unselective antagonist, respectively. Atropine (30 micrograms/kg) significantly delayed the onset of the next complex. On the contrary, pirenzepine displayed a biphasic action: low doses (less than 100 micrograms/kg) shortened the cycle period, whereas at 300 micrograms/kg the drug behaved like atropine. Pirenzepine affected the cycle period in the low-dose range by reducing the length of phase I. Both atropine and pirenzepine impaired the migration of the ongoing complex, and significantly reduced the migration velocity of the following one. These findings suggest that the initiation of the migrating myoelectric complex in the dog is under an inhibitory influence mediated by the M1 muscarinic receptor subtype; on the other hand, M2 receptor activation is needed for the onset of the activity front. Finally, both receptor subtypes determine the normal migration of phase III.

Animals↗
PubMed1986

Serotonin increases the velocity of propagation and frequency of the migrating myoelectric complexes.

The effect of serotonin on the myoelectric activity of the gastrointestinal tract was evaluated in seven opossums. Continuous intravenous administration of serotonin reduced the cycle duration of the migrating myoelectric complex and increased the velocity of propagation of the phase III. These changes were dose-dependent and were observed only with high doses of serotonin of 0.1 mg kg-1 h-1 or more. Infusion of 0.01 mg kd-1 h-1 had no effect on the motility of the gastrointestinal tract. The motility changes occurred in all segments of the gastrointestinal tract studied and were characterized by a continuous and organized increase in the velocity of propagation of the activity front (phase III) of the migrating myoelectric complex from the antrum to the terminal ileum. The cycle duration of the two migrating myoelectric complexes following administration of methysergide at 1.0 mg kg-1 was similar to the control migrating myoelectric complexes. We concluded that continuous infusion of serotonin in the opossum increases the velocity of propagation of the phase III of the migrating myoelectric complex from the antrum to the terminal ileum.

Animals↗
PubMed1991

Neuromedin-N inhibits migrating myoelectric complex and induces irregular spiking in the small intestine of rats; comparison with neurotensin.

The effects of neuromedin-N on migrating myoelectric complexes in the small intestine of rats were studied. As neuromedin-N and neurotensin are structurally related peptides a comparison with neurotensin was made. Myoelectric activity was recorded by means of three bipolar electrodes implanted into the wall of the small intestine at 5, 15 and 25 cm distal to the pylorus. The peptides were administered as intravenous infusions to fasted conscious rats. Neuromedin-N at doses of 100-800 pmol kg-1 min-1 caused a dose-dependent disruption of the migrating myoelectric complexes and induced irregular spiking activity (n = 7, P less than 0.05). Neurotensin induced a similar response, but at doses of 1.0-8.0 pmol kg-1 min-1 (n = 5, P less than 0.05). Thus, on a molar basis, neuromedin-N appeared to be about 100-times less potent than neurotensin. Hexamethonium (20 mg kg-1 i.v.) inhibited the migrating motor complexes and induced quiescence, but did not block the effect of neuromedin-N at a dose of 800 pmol kg-1 min-1. Atropine (1 mg kg-1 i.v.) and mepyramine (2 mg kg-1 i.v.) did not affect the migrating motor complexes, nor did they block the effect of neuromedin-N. Simultaneous infusion of neuromedin-N and neurotensin in a 1:1 molar ratio at doses of 2 pmol kg-1 min-1 showed inhibition of the response to neurotensin in eight out of ten experiments. In conclusion, neuromedin-N changes the myoelectric activity in the small intestine from a fasting to a fed pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1992

Locus ceruleus modulates migrating myoelectric complex in rats.

The role of the locus ceruleus (LC) in the control of migrating myoelectric complex (MMC) was investigated in rats with lesions induced by injections of 6-hydroxydopamine (6-OHDA). Control animals received the vehicle alone. MMC was recorded in conscious rats chronically fitted with electrodes. After 6-OHDA was injected into the LC, lesions of the LC were total, partial (mostly rostral), or ineffective. The MMC period was significantly longer in animals with a total or partial lesion but was unchanged in animals with an ineffective lesion. No lesion of other brain noradrenergic nuclei was observed. The longer MMC period is comparable to that obtained after intracerebroventricular injection of 6-OHDA, which is responsible for a more diffuse destruction of brain noradrenergic systems, including LC itself. Bilateral lesions of the central tegmental tract, which carries ascending noradrenergic axons from the medullary and pontine cell groups outside the LC, do not alter the MMC cycle. Consequently, the LC is most likely the major brain noradrenergic candidate for modulating the MMC pattern in rats.

Animals↗
PubMed1984

Motilin and migrating myoelectric complexes in the pig and the dog.

Associations between migrating myoelectric complexes (m.m.c.s) and peak plasma motilin concentrations were confirmed in the dog fasted 18 h and shown not to be present in pigs fasted 3-4 h. Infusions of both natural porcine and synthetic 13-Nle-motilin failed to induce m.m.c.s in the pig. It was confirmed that motilin infusions stimulated the premature appearance of m.m.c.s in the dog whether motilin remained within, or exceeded, its normal plasma values. Immunoneutralization by intravenous administration of rabbit antimotilin serum was without effect on naturally occurring m.m.c.s in the dog and the pig. In the dog, antimotilin serum blocked production of m.m.c.s by exogenous motilin for 7-10 d post-immunoneutralization. It is suggested that there are both: (i) species differences in associations of m.m.c.s and plasma motilin concentration, and (ii) an independence of m.m.c.s from plasma motilin even in the dog in which normally exogenous motilin can produce m.m.c.s.

Animals↗
PubMed1981

Intrinsic nervous control of migrating myoelectric complexes.

The role of intrinsic nerves in the control of migrating myoelectric complexes (MMCs) was studied in seven conscious dogs, each implanted with a set of eight bipolar Trimel wire electrodes. Local areas, 3-5 cm long, were perfused close intra-arterially via an exteriorized heparinized Silastic cannula. Experiments consisted of giving bolus injections of atropine (20-50 micrograms), hexamethonium (20 mg), and tetrodotoxin (TTX; 3-30 micrograms) via the catheter at varying periods of time with respect to the arrival of phase III at the perfused site. Atropine and hexamethonium, given close intra-arterially immediately before the arrival of phase II at the perfused site, blocked its further propagation. Tetrodotoxin given locally also blocked the propagation of phage III, as above. After the block, TTX initiated a new phase III activity at, or distal to, the perfused site in 10 out of 14 perfusions. The new phase III activity propagated distally. This study shows that the mechanisms for the initiation and propagation of MMCs are built into the enteric plexus. Once an MMC is initiated, its propagation is achieved by proximal-to-distal excitation through the intrinsic cholinergic network of neurons. This study explains the lack of any significant changes in the propagation parameters of MMCs after vagotomy or celiac and superior mesenteric ganglionectomy.

Animals↗