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Results for “Myoelectric Complex, Migrating”

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PubMed1996

Effect of motilin on gastrointestinal myoelectric activity in conscious rabbits.

Gastrointestinal myoelectric activity was investigated in conscious rabbits with chronically implanted electrodes. As rabbit stomach is never empty, food was removed 1 h before the beginning of recordings. Propagated activity fronts spontaneously started in the jejunum without associated changes in the antroduodenal area. Intravenous administration of either motilin (600-1500 ng/kg) or erythromycin (5-50 micrograms/kg) did not modify antral activity, but simultaneously increased duodenal and jejunal activity in a dose-dependent manner. Spontaneous and induced jejunal activity fronts showed some similarities. However, those induced did not propagate and were not followed by a quiescence period. The effects of motilin (900 ng/kg) and erythromycin (25 micrograms/kg) were resistant to atropine (0.5 mg/kg), hexamethonium (2 mg/kg), or ondansetron (0.5 mg/kg). These results suggest that motilin is not a physiological modulator of the migrating myoelectric complex (MMC) in rabbits. Moreover, neither cholinergic nor 5-HT3 receptors are involved in either motilin or erythromycin-induced actions.

Animals↗

PubMed1992

Effect of infusion of a diarrheogenic dose of PGE2 on gastrointestinal electrical activity in the conscious piglet.

In 5 conscious piglets with electrodes implanted on the antrum pylori and small intestine, phasic and integrated electrical activity was daily recorded. PGE2, 10 micrograms/kg/min, was infused intravenously during 1.5 h and the induced changes in electrical activity were analyzed. Clinical appearance was also studied. PGE2 induced an inhibition in both antral and intestinal activity. In the antrum this inhibition was characterized by a decrease in the frequency of electrical control activity and fast oscillations, and an increase in the duration of the inhibitory phase. Small intestinal recordings revealed an increase in the quiescence phase for the duodenum and a decrease in the integrated total activity for the duodenum, jejunum and ileum, induced by a decrease in phase II activity. PGE2 was without influence on phase III activity and the recycling of the migrating myoelectrical complexes. All piglets developed a severe diarrhea. Vomiting, sedation, fever and shivering were observed in most animals. These data suggest that the diarrheogenic effect of PGE2 is not provoked by an increase in small intestinal motility. Moreover, the direct effect of this PG is a partial inhibition of gastrointestinal electrical activity.

Animals↗

PubMed1992

Influence of PGF2 alpha on gastrointestinal activity in the conscious piglet.

In 5 conscious piglets with electrodes implanted on the antrum pylori, duodenum, jejunum and ileum, the effect of intravenous infusion of PGF2 alpha, 1 and 10 micrograms/kg/min during 2 h, on gastrointestinal electrical activity was studied. The influence of the PG, 10(-8) to 10(-4) M, on longitudinal tissue strips from the same segments was also examined. The in vitro results demonstrate that PGF2 alpha has only a weak contractile effect on duodenal and jejunal strips. This effect was enhanced in the presence of atropine and indomethacin. In the in vivo part of the study PGF2 alpha induced an inhibition of antral electrical activity as evidenced by a prolongation of the inhibitory phases and a reduction of the frequency of the fast oscillations. In the small intestine only ileal activity was changed significantly. PGF2 alpha provoked an increase in the phase II or irregular spiking activity and an increase in the interval of the migrating myoelectrical complexes in this segment.

Animals↗

PubMed2004

Effects of peritoneal injury and endotoxin on myoelectric activity and transit.

BACKGROUND: The combined effects of peritoneal injury and intraabdominal infection on gastrointestinal motility in postoperative ileus are poorly understood MATERIALS AND METHODS: Sprague Dawley rats underwent placement of three electrodes on the small intestine and a tube gastrostomy. Animals were divided into four groups: a control (n = 12), a peritoneal injury (PI, n = 12), a peritoneal injection of lipopolysaccharide (LPS, n = 12), and a LPS + PI group (n = 12). After myoelectric activity recording on postoperative day (POD) 1, half of the rats in each group underwent intestinal transit studies. The remainder of the rats underwent another myoelectric activity recording as well as intestinal transit study at 48 h after operation RESULTS: Although six to eight of rats in the control, PI, and LPS groups recovered migrating myoelectric complex (MMC) on POD 1, no rats in the LPS + PI group recovered MMC by POD 1. The transit distance on POD 1 in the PI (36 +/- 2.5 cm) and LPS + PI group (38 +/- 2.8 cm) was shorter than that in the control group (53 +/- 2.0 cm, P < 0.05) CONCLUSIONS: Full recovery of liquid intestinal transit precedes the return of MMC activity after abdominal surgery in the rats. Peritoneal injury causes decreased intestinal transit and when combined with intraabdominal injection of LPS may cause the delayed recovery of MMC activity.

Abdomen↗

PubMed2004

Ghrelin stimulates motility in the small intestine of rats through intrinsic cholinergic neurons.

BACKGROUND AND PURPOSE: Ghrelin is a peptide discovered in endocrine cells of the stomach. Since ghrelin mRNA expression and plasma levels are elevated in the fasting state, we investigated the effects of ghrelin on the interdigestive migrating myoelectric complex (MMC) in the small intestine in vivo and compared with motor effects of ghrelin in vitro. METHODS: Sprague-Dawley rats were supplied with a venous catheter and bipolar electrodes in the duodenum and jejunum for electromyography of small intestine in awake rats. In organ baths, isometric contractions of segments of rat jejunum were studied. RESULTS: Ghrelin dose-dependently shortened the MMC cycle length at all three recording points. At the duodenal site, the interval shortened from 17.2+/-2.0 to 9.9+/-0.8 min during infusion of ghrelin (1000 pmol kg(-1) min(-1)) and at the jejunal site from 17.5+/-2.2 to 10.5+/-0.8 min. Ghrelin contracted the muscle strips with a pD2 of 7.97+/-0.47. Atropine (10(-6) M) in vitro and (1 mg kg(-1)) in vivo blocked the effect of ghrelin. CONCLUSION: Ghrelin stimulates interdigestive motility through cholinergic neurons. Ghrelin also stimulates motility, in vitro, suggesting that ghrelin receptors are present in the intestinal neuromuscular tissue and mediate its effects via cholinergic mechanisms.

Animals↗

PubMed1993

Ketorolac prevents postoperative small intestinal ileus in rats.

The effect of ketorolac, a parenterally administered, nonsteroidal anti-inflammatory drug, was examined in a rat model of postoperative ileus. Small intestinal transit was measured by calculating the geometric center (GC) of distribution of 51CrO4. Laparotomy significantly delayed transit (GC: 2.2 +/- 0.2 after laparotomy versus 5.6 +/- 0.5 for unoperated controls, p < 0.01). The administration of ketorolac (1 mg/kg) improved the GC to 5.2 +/- 0.2 (p < 0.01), indicating normal intestinal transit after surgery in ketorolac-treated animals. Small intestinal myoelectric activity was recorded in rats with implanted electrodes. Animals treated with saline 2 hours postoperatively did not show return of the migrating myoelectric complex (MMC) in 183 +/- 25 minutes. In contrast, rats receiving ketorolac postoperatively had return of MMC activity in 59 +/- 18 minutes (p < 0.01). Preoperative ketorolac treatment reduced the duration of MMC inhibition after surgery from 197 +/- 55 minutes to 13 +/- 5 minutes (p < 0.05) when compared with saline. In summary, ketorolac hastens the return of MMC activity when given postoperatively. When ketorolac is administered preoperatively, it completely prevents the delay in intestinal transit and the inhibition of myoelectric activity seen in postoperative ileus. We concluded that ketorolac may be of benefit in the prevention and treatment of postoperative ileus.

Animals↗

PubMed1996

Gastrointestinal myoelectric activity during endotoxemia.

BACKGROUND: Gastrointestinal myoelectric activity during postoperative ileus has been well characterized. However, the common clinical scenario of ileus occurring during and after episodes of sepsis is not well understood. The aim of our study was to determine the effects of a single, sublethal dose of endotoxin on canine gastrointestinal myoelectric activity. METHODS: Eight dogs underwent placement of serosal electrodes on the stomach and small intestine and insertion of a jejunal cannula. After the animals recovered, electrical activity and jejunal mucosal blood flow were determined during fasting and with feeding. Following completion of these baseline studies dogs were given a single, sublethal dose of Escherichia coli lipopolysaccharide (200 g/kg) intravenously, and the studies were repeated daily for 3 consecutive days. RESULTS: Endotoxin resulted in an absence of the interdigestive migrating myoelectric complex for 2 days, a decrease in duodenal and jejunal action potentials during fasting and with feeding, but no decreases in jejunal mucosal blood flow. The gastrointestinal myoelectrical patterns returned to those found in health on postendotoxin day 3. CONCLUSIONS: A single, sublethal dose of endotoxin results in a temporary disruption of gastrointestinal myoelectric activity similar to that seen during postoperative ileus. The etiology of this "adynamic" ileus is unknown but does not appear to be secondary to intestinal ischemia.

Action Potentials↗

PubMed1992

Involvement of hypothalamic noradrenergic systems in the modulation of intestinal motility in rats.

Selective lesions of the noradrenergic systems of the paraventricular nucleus (PVN) of the hypothalamus with 6-hydroxydopamine (6-OHDA) lengthen the periodicity of the migrating myoelectric complex (MMC), an index of intestinal motility, in rats. These lengthening effects resemble those obtained after lesions of the locus coeruleus (LC), thus suggesting that noradrenergic terminals from LC to the PVN are involved in this modulation.

Analysis of Variance↗

PubMed1997

Disrupted bile flow affects interdigestive small bowel motility in rats.

BACKGROUND: The role of bile flow in the regulation of small bowel motility and the migrating myoelectric complex (MMC) is unclear. We aimed to study the effects of biliary diversion or obstruction on the MMC in a newly developed rat model. METHODS: In rats, myoelectrodes were implanted in the jejunum, and the proximal common bile duct (CBD) was cannulated and exteriorized at the head, enabling us to manipulate biliary flow without influencing pancreatic flow and without the need of anesthesia or additional surgery. Group A were controls without CBD cannulas. Biliary circulation was exteriorized but kept intact in group B; bile was diverted externally in group C; and the CBD was obstructed in group D. MMCs were recorded in unrestrained conditions by jejunal electromyography before and after biliary diversion or obstruction. Spontaneous recanalization of the CBD was monitored by measurement of serum bilirubin and by cholangiography. RESULTS: Exteriorization of the CBD without interruption of bile flow did not affect MMC duration (group A, 17.3 +/- 0.3 minutes [mean +/- SEM]; group B, 16.5 +/- 0.6 minutes). MMCs disappeared temporarily after CBD obstruction but not after biliary diversion. MMCs of increased duration were seen after 1 day in rats with biliary diversion or CBD obstruction (group C, 26.1 +/- 4.4 minutes; group D, 36.3 +/- 4.8 minutes [p < 0.05]). MMCs after biliary diversion or obstruction were characterized by an increased duration of phase II-like activity and decreased duration of phase I activity. CONCLUSIONS: We conclude that MMCs disappear temporarily early after CBD obstruction, but MMCs of increased duration are seen after 1 day of biliary diversion or obstruction. Thus disrupted bile flow affects interdigestive small bowel motility in rats.

Animals↗

PubMed2001

The inhibitory mechanism of GLP-1, but not glucagon, on fasted gut motility is dependent on the L-arginine/nitric oxide pathway.

Effects of glucagon-like peptide-1 (GLP-1) and glucagon on fasted gut motility in conscious rats were investigated as regards dependence on nitric oxide (NO). Small bowel motility was studied by electromyography and a jugular vein catheter was implanted for administration of drugs. GLP-1 (5-40 pmol x kg(-1) x min(-1)) prolonged the cycle length and abolished phase III of the migrating myoelectric complex (MMC) (P<0.01). Low doses of GLP-1 did not affect duration, propagation velocity or calculated length of phase III. At 1 mg x kg(-1) N(omega)-nitro-L-arginine (L-NNA) blocked the GLP-1 response up to a dose of 10 pmol x kg(-1) x min(-1) (P<0.05), while higher doses were able to overcome L-NNA-induced disinhibition of the GLP-1 response (P<0.05). Similarly, L-arginine at 300 mg x kg(-1) prevented L-NNA-induced disinhibition of the GLP-1 response (P<0.05). Glucagon (200-1000 pmol x kg(-1) x min(-1)) prolonged the cycle length and abolished phase III of MMC (P<0.01) independent of NO. Again, low doses of glucagon did not affect duration, propagation velocity or calculated length of phase III. In conclusion, inhibition of fasted motility by GLP-1 at low doses is dependent on NO, while high doses of GLP-1 and glucagon exert effects on motility independently from NO.

Animals↗

PubMed1997

Effect of L364718 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 mumol kg-1 inhibited exogenous CCK-8-induced pancreatic exocrine secretion. Intravenous infusion of the antagonist at 2.45 mumol 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.

Animals↗

PubMed2002

Different endogenous opioid effects on delta- and mu-receptor subtypes in antral and duodenal motility of conscious dogs.

To evaluate the role of endogenous opioids in regulation of upper gastrointestinal motility in unanesthetized dogs and to differentiate the actions on mu- and delta-opioid receptors, seven strain gauges and five platinum electrodes were chronically implanted at the serosa along the antrum and duodenum and connected to a plug in the neck of the dog. Signals were processed by a Hellige AC amplifier, a rectilinear recorder, and a data aquisition system. A motility index (MI) was calculated and together with the electrical data a contractile activity percentage (CAP) was determined for consecutive 30 min periods. The delta-opioid antagonist ICI 741 864 and the mu-receptor blocker naloxone were injected intraarterially through a chronic Groshong catheter placed in the pyloric region and connected to a subcutaneous port. After a meal of solid food, ICI 174 864 increased motility relative to controls in the antrum averaged over 5 hr by 144.4%+/-26 for the MI and 73%+/-26 for CAP; after naloxone MI increased by 222%+/-60 and CAP 121%+/-76. In the duodenum, ICI 174 864 decreased MI over a range of 57% to 22% (P < 0.05). Naloxone increased MI and CAP significantly after 2.5 hr. We interpreted the results of ICI 174 864 in the duodenum to reflect suppression of a tonic opioid influence at the delta-receptor mainly at the prevertebral ganglion. In the interdigestive state in 56% of the dogs, naloxone delayed the occurrence of phase III of the migrating myoelectric complex (MMC) for up to 370 min, while under ICI 174 864, normal interdigestive cycles were present. Disturbance of the timing of the interdigestive cycles at central mu-opioid receptors may by involved in the effect.

Animals↗

PubMed1991

Correlation of the gastric emptying of nondisintegrating tablets with gastrointestinal motility.

The aim of the present study was to correlate the gastric emptying (GE) of nondisintegrating tablets with changes in gastrointestinal (GI) motility. Eight, healthy, male subjects each received 5 x 7-mm radiolabeled tablets, a radiolabeled meal, and a radiotelemetry capsule (RTC). Transit of the radiolabeled formulations was followed by gamma scintigraphy and the RTC detected contractile activity in the GI tract. The study demonstrated that 7-mm tablets can empty from the fed stomach, prior to the onset of interdigestive activity. Those tablets that were not emptied during fed activity were retained through the period of quiescence associated with the onset of the migrating myoelectric complex (MMC) and left the stomach during contractions associated with phase 2 and 3 activity. The RTC was retained in the stomach and was emptied only by large phase 3 contractions commonly termed the "housekeeper" wave. However, in one subject, the RTC was retained in the stomach for over 12 hr, during which time three distinct phase 3 complexes were monitored.

Adult↗

PubMed1997

Submandibular gland peptide-T (SGP-T) inhibits intestinal anaphylaxis.

A novel peptide, submandibular gland peptide-T (SGP-T), which reduces allergen-induced hypotension, was examined for effects on intestinal anaphylaxis. Hooded-Lister rats were sensitized to egg albumin and prepared for the measurement of in vivo myoelectric activity of the jejunum. The disruption of migrating myoelectric complexes (MMCs) that occurs upon intraluminal, duodenal challenge with antigen of sensitized rats was inhibited by 75% upon intravenous treatment with 100 micrograms/kg of SGP-T. In addition, SGP-T reduced the number of rats experiencing anaphylactic diarrhea and disrupted MMCs, but the peptide did not alter antigen-provoked release of rat mast cell protease II. The mechanism of action of SGP-T remains to be determined, but it apparently does not act directly on mast cells to exert its antianaphylactic action. These results emphasize that modulation of immediate hypersensitivity reactions is only one of several gastrointestinal activities that are affected by growth factors and peptides released from salivary glands.

Anaphylaxis↗

PubMed1997

Endotoxin actions on myoelectric activity, transit, and neuropeptides in the gut. Role of nitric oxide.

The lipopolysaccharide (endotoxin) of gram-negative bacteria has systemic effects in animals and man. Our aim was to investigate the effects of E. coli lipopolysaccharide on motility and transit through the small intestine in rats and to analyze plasma and tissue concentrations of intestinal neuropeptides. When lipopolysaccharide (20-160 micrograms/kg) was administered intravenously, the migrating myoelectric complex was replaced by spike bursts accompanied by rapid transit. Tissue concentrations of substance P and neurokinin A decreased, while plasma levels of calcitonin gene-related peptide increased N omega-Nitro-L-arginine, N omega-L-arginine methyl ester, dexamethasone, or indomethacin prevented these changes in myoelectric activity and tissue contents of neuropeptides. All of these compounds, except indomethacin, prevented the increased rate of transit. Thus, lipopolysaccharide changes motility through the nitric oxide and arachidonic pathways, resulting in rapid transit through the gut.

Animals↗

PubMed1998

Mediation of irregular spiking activity by multiple neurokinin-receptors in the small intestine of the rat.

1. We have studied the small intestinal myoelectric response to the natural tachykinins substance P (SP), neurokinin A (NKA), neurokinin B (NKB), and the neurokinin-receptor selective agonists substance P methyl esther (SPME), [beta-Ala8]neurokinin A 4-10, and senktide in conscious rats. 2. The effects of the agonists were studied before and after administration of the selective neurokinin2 (NK2)-receptor antagonist MEN 10,627. 3. Under basal conditions SP, NKA, NKB, as well as the selective NK1-receptor agonist SPME, the NK2-receptor agonist [beta-Ala8]NKA 4-10, and the NK3-receptor agonist senktide, disrupted the interdigestive rhythm with regularly recycling migrating myoelectric complexes and induced a phase II-like irregular spiking activity. 4. MEN 10,627 given alone did not affect the interdigestive rhythm. 5. MEN 10,627 inhibited the response to [beta-Ala8]NKA 4-10 but not to SP, SPME, NKA, NKB or senktide. 6. It is concluded that not only NK2 receptors, but also other receptors, such as NK1 and NK3 receptors, may mediate the motility-stimulating action of different tachykinins in vivo. 7. It is further concluded that MEN 10,627 exerts a selective NK2-receptor antagonism, and may be a valuable tool for assessing the functional role of NK2-receptors in gastrointestinal physiology.

Animals↗

PubMed2000

Alterations of intestinal motor responses to various stimuli after Nippostrongylus brasiliensis infection in rats: role of mast cells.

Nippostrongylus brasiliensis infection induces jejunal mastocytosis associated with enteric nerve remodelling in rats. The aim of this study was to evaluate the intestinal motility responses to meals and to neurotransmitters involved in the control of gut motility (acetylcholine (carbachol), substance P and neurokinin A) in both control and N. brasiliensis-infected rats 30 days post-infection. All rats were equipped with NiCr electrodes in the jejunum to record myoelectrical activity. The duration of disruption of the jejunal migrating myoelectrical complexes (MMC) induced by the different stimuli was determined. Meal ingestion and substance P administration disrupted the MMC pattern for similar durations in the two groups. Carbachol and neurokinin A induced a significantly longer MMC disruption in post-infected rats than in controls (125 +/- 8.3 vs. 70 +/- 6 min for carbachol 100 microg kg-1 and 51 +/- 4 vs. 40 +/- 2 for neurokinin A 50 microg kg-1). The enhanced motor response in postinfected rats was reduced by previous mast cell stabilization with ketotifen or mast cell degranulation with compound BrX 537 A. In conclusion, the increased intestinal motor reactivity to carbachol and neurokinin A in post-N. brasiliensis-infected rats depends upon intestinal mast cell hyperplasia and degranulation.

Animals↗

PubMed2002

Automated, quantitative analysis of interdigestive small intestinal myoelectric activity in rats.

Quantitative analysis of myoelectric activity (EMG), to investigate small intestinal motility in rats, is normally based on manual classification into sequences of phase I, phase II and phase III. This classification is partly subjective. We aimed to develop a more objective method for the analysis of the migrating myoelectric complex (MMC). From the EMG, a derived signal is calculated as a measure of activity. Depending on the level of this derived signal, the EMG is classified into 'quiescent phase', 'irregular phase' or 'activity front'. The threshold levels for these phases are automatically calculated from the EMG data. A proposal for subdivision into MMCs is automatically generated. To calculate MMC length, the user must manually reject nonpropagated activity fronts. While developing the method, more than 19 derived signals were tested. These included variants of spike frequency, signal power and spike-burst length. The spike frequency signal was chosen because it gave minimal deviation from manual classification. Using the new automated method, recordings from the jejunum of 15 healthy rats were analysed (6 h each). The calculated phase lengths were consistent with the results of manual analysis. The presented method allows objective analysis of the interdigestive EMG signals of the small intestine.

Action Potentials↗