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At least 19 recordsLinked to original sources
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↗
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↗
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↗
PubMed1985

Dose- and time-dependent biphasic response to morphine on intestinal migrating myoelectric complex.

We investigated the biphasic response to morphine infusion on migrating myoelectric complex (MMC) cycling in seven conscious dogs. Morphine infusions at the rate of 20, 50, 100, 200, 500 and 1000 micrograms/kg/hr were started at 0 or 40% of MMC cycle and continued for 3 hr in each experiment. All infusion rates starting at 40% of MMC cycle initiated the first postinfusion MMC cycle prematurely (P less than .05). The mean period of the first postinfusion MMC cycle decreased for higher infusion rates. After the first premature MMC cycle, higher infusion rates (500 and 1000 micrograms/kg/hr) inhibited MMC cycling completely whereas the lower infusion rates inhibited MMC cycling in a dose-dependent manner. When infusion was started at 0% of MMC cycle, the first premature MMC cycle occurred consistently only at 20 micrograms/kg/hr. For higher infusion rates, initiation of premature MMC cycle or inhibition of MMC cycling was dose-dependent. Naloxone blocked both the excitatory and the inhibitory effects of morphine on MMC cycling. Morphine infusions also initiated phase III activity in the postprandial state in a dose-dependent manner. Truncal vagotomy and splanchnectomy did not abolish the excitatory or the inhibitory effects of morphine on MMC cycling. We conclude that morphine infusion has a biphasic effect on MMC cycling. The exact nature of the response depends on the dose of morphine and the time in the MMC cycle when infusion is started. Both the excitatory and the inhibitory responses may be mediated through peripheral mu opiate receptors.

Animals↗
PubMed1990

[The effect of microinjections of bombesin into the amygdala on the slow-wave frequency of the gastroduodenal smooth muscles and on the migrating myoelectric complex].

In dogs with electrodes implanted in the smooth muscle wall of the stomach and duodenum, microinjection of bombesin (5 micrograms) during the 2nd phase of the migrating myoelectric complex decreased frequency of slow waves in the stomach, leaving unaltered the frequency of slow waves in the duodenum. Bombesin caused a short-term inhibition of the gastric and intestinal spike activity followed by its increase, the active period of the migrating myoelectric complex being prolonged.

Amygdala↗
PubMed1992

The role of migrating myoelectric complexes in the regulation of digesta transport in the preruminant calf.

Four calves were equipped with an electromagnetic flow probe inside the transverse duodenum and with electrodes at intervals of 2 cm on either side of the probe. Amounts of 0.5, 2.0, 3.5, and 5.0 kg of whole milk were given according to a latin square design. Recordings of digesta flow and myoelectric activity were made during a 5.6-h period after feeding to quantify the influence of migrating myoelectric complexes on digesta flow through the transverse duodenum of preruminant calf under different levels of milk intake. Immediately after feeding, a phase of irregular spiking activity appeared; its length increasing linearly (p = 0.002) with the amount of milk fed. Increasing milk intake led to linear increases in duration (p = 0.001) and total electrical activity (p = 0.002) of the irregular activity phases, quadratic shortening of the quiescent phases (p = 0.021), and linear decrease (p = 0.006) in the numbers of migrating myoelectric complexes. Intermittent flows of digesta, each of them corresponding to a strong spike burst, appeared during irregular spiking activity phases. Augmentation of the milk ingested did not affect the volume of each gush of digesta but caused a cubic increase in the number of gushes (p = 0.023) and in the total volume of digesta (p = 0.009). These cubic effects implied that with increased intake of milk, the duodenum endeavoured to accelerate the flow of digesta in an attempt to return to an "empty state" in about the same time for all levels of milk consumed. This was achieved mainly through adjustments in the duration and activity of the irregular spiking activity phase.

Animals↗
PubMed1991

Modulation of the migrating myoelectric complex by brain noradrenergic systems in rats.

The respective role of central and peripheral noradrenergic systems in the control of migrating myoelectric complex (MMC) was investigated in rats following lesions with 6-hydroxydopamine (6-OHDA). 6-OHDA was injected via intraperitoneal (ip), intracisternal (icis), and intracerebroventricular (icv) routes in rats. Control animals received the vehicle alone. One month later, MMC was recorded in conscious rats chronically fitted with electrodes. The MMC period was significantly lengthened after 6-OHDA ip or icv injection, and slightly shortened after 6-OHDA icis injection. No disruption of central noradrenergic systems was detected after ip lesions. Norepinephrine content was reduced in the digestive tract after ip lesions, in the spinal cord after icis lesions, and in the cortex, the hypothalamus, pons-medulla, and the spinal cord after icv lesions. After icis lesions, noradrenergic perikarya were spared in pons-medulla, whereas only pons noradrenergic perikarya were lesioned after icv lesions. We conclude that lesions of brain noradrenergic systems modify MMC periodicity in rats. The rostral noradrenergic systems may play the major modulatory role.

Animals↗
PubMed1977

Migrating myoelectrical complex of the small intestine. An intrinsic activity mediated by the vagus.

In healthy conscious parenterally fed dogs and in sheep on their usual diet, the basic motor profile on the small intestine consists of recurring cycles of action potential activity. This cyclic pattern called the migrating myoelectrical complex comprises two distinct phases termed irregular, and regular spiking activity and is followed by a period of quiescence. The pattern persists after bilateral transthoracic vagotomy and in animals rendered diabetic by alloxan. In dogs, feeding disrupts the migrating myoelectrical complex pattern by obliterating the phases of regular spiking activity and quiescence for 6 to 12 hr, depending upon the amount of dry matter intake. After vagotomy a latency in the disruption of the migrating myoelectrical complex pattern with feeding occurs and in vagotomized dogs rendered diabetic, the duration of disruption is strongly reduced. In sheep, the duration of irregular spiking activity of a jejunal segment increased or decreased corresponding to the bulk of digesta, a phenomenon damped after vagotomy. The results indicate that the role of the vagus is limited to (1) prompting prandial disruption, which is then maintained by hormonal effect; (2) regulating the irregular spiking activity duration in relation to the bulk of digesta.

Action Potentials↗
PubMed1991

Variation of slow-wave frequency and locking during the migrating myoelectric complex in dogs.

Slow waves determine rhythm and polarity of spike bursts. We measured the variation of slow-wave frequency (swf) and locking (swl) in the canine jejunum during the various phases of the migrating myoelectric complex (MMC) and during induced phase III (erythromycin 125 micrograms/kg iv bolus or somatostatin 2.5 micrograms.kg-1.h-1 iv infusion), blocked phase III (atropine 20 micrograms/kg iv bolus), and so-called stationary phase III activity (cisapride 150 micrograms/kg iv bolus). The EMG of 4 dogs, implanted with 10 bipolar electrodes, was recorded on a polygraph. Our results indicate that swf and swl change during the MMC from a stepwise swf gradient with slow waves locked in plateaus during phase I to a continuous swf gradient without or with significantly reduced phase locking during phase III. The length of the first swf plateau decreases significantly from 42 +/- 12 cm post Treitz during phase I to 11 +/- 4 cm during spontaneous phase III. Atropine block of phase III activity prevents phase unlocking and development of a continuous swf gradient. Our hypothesis is that phase unlocking may be one of the induction mechanisms of spike-burst activity.

Animals↗
PubMed1989

[Effects of human chorionic gonadotrophin and progesterone on small intestinal migrating myoelectric complex in rats].

The effects of human chorionic gonadotrophin (HCG) and progesterone (P) on migrating myoelectric complex (MMC) of the small intestine in ovariectomized rats were investigated by implanted monopolar-electrode in the intestinal wall of the duodenum, jejunum and ileum. The results showed (1) after i.v. administration of HCG the periodicity of the duodenal and upper jejunal MMC was interrupted by irregularly prolonged phases II occurring intermittently; (2) after i.m. administration of P the duration of phases I and II of the duodenal MMC was significantly prolonged, but the periodicity was not affected; (3) the effect of P plus HCG on MMC was similar to that of HCG alone, but the combined effect was spread over the whole small intestine. These results suggest that HCG can induce remarkable changes of the small intestinal MMC, which are similar to those observed in pregnant rats. In the presence of P, the effect of HCG is enhanced markedly.

Animals↗
PubMed1989

Opioid receptors and the initiation of migrating myoelectric complexes in dogs.

The role of endogenous opioids and opioid receptors in the control of migrating myoelectric complexes (MMCs) was studied in conscious dogs implanted with silver-silver chloride electrodes. In normal fasted dogs, MMC cycle times were 103 +/- 7 min in the duodenum. During naloxone infusion (1-2 mg/kg iv, then 0.2-1.0 mg.kg-1.h-1 iv) cycle times increased to 219 +/- 29 min (P less than 0.01). Naloxone (2 mg/kg iv, then 1 mg.kg-1.h-1 iv) had no effect on the response of the small intestine to bethanecol (5 mg sc) or to feeding. Pretreatment with naloxone (2 mg/kg iv) 5 min before the administration of motilin (400-500 micrograms/kg iv) did not block the initiation of MMCs by motilin. In separate experiments, animals were pretreated with the positive or negative isomer of the opioid receptor antagonist WIN-44,441 (0.2 mg/kg iv) 5 min before morphine administration. The negative isomer binds to opioid receptors whereas the positive isomer does not. The negative but not the positive isomer antagonized all effects of morphine on intestinal myoelectric activity. These studies suggest that endogenous opioids and opioid receptors may play a role in control of the initiation of MMCs and that motilin and exogenous opioids act via different mechanisms to initiate MMCs.

Animals↗