[Gastrointestinal motility after total gastrectomy--influence of the reconstruction of the stomach with the jejunum on the migrating myoelectric complex].
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Animals↗
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Results for “Myoelectric Complex, Migrating”
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Feeding disrupts the migrating myoelectric complex: is insulin the cause? [proceedings].
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Animals↗
Myoelectric motility patterns following open versus laparoscopic cholecystectomy.
Laparoscopic surgery is associated with a lack of postoperative ileus. To determine if differences exist in postoperative motility patterns, 8 dogs were instrumented with bipolar electrodes 10-14 days prior to open (n = 4) or laparoscopic (n = 4) cholecystectomy. In both groups, Phase II activity disappeared in the first 24 h after operation. The appearance of the migrating myoelectric complex in the small intestine and the migrating colonic complex were used as criteria for recovery from postoperative ileus. Postoperative migrating myoelectric complex cycle length, migrating myoelectric complex, migration velocity, and colonic spike bursts/hour were also measured. No statistically significant differences were observed between groups in study parameters examined. Postoperative myoelectric motility patterns in dogs undergoing open versus laparoscopic cholecystectomy are not different. Other factors may be responsible for the rapid return to oral intake following laparoscopic cholecystectomy.
Animals↗
Myoelectric correlates of colonic motor complexes and contractile activity.
This report describes the myoelectric correlates of colonic motor complexes and contractile activity. A set of four bipolar electrode/strain-gauge pairs was surgically implanted on the colon of each of the five dogs used in this study. Each recording site showed a cyclic occurrence of bursts of contractions called contractile states. The colonic muscle contracted mainly at two frequencies during a contractile state, long-duration contractions at 0.5-2 cycles/min and short-duration contractions at 4-6 cycles/min. The long-duration contractions at 0.5-2 cycles/min were associated with bursts of contractile electrical complex (electrical oscillations at 25-40 cycles/min) and continuous electrical response activity on a 1:1:1 basis. The short-duration contractions at 4-6 cycles/min were associated with bursts of discrete electrical response activity on a 1:1 basis. Those episodes of contractile electrical complex, continuous electrical response activity, and discrete electrical response activity that migrated orad or aborad over at least half the length of the colon were called colonic migrating myoelectric complexes. All other patterns of occurrence of these episodes were called colonic non-migrating myoelectric complexes. A total of 184 colonic migrating myoelectric complexes were recorded during a total recording period of 148 h: 173 migrated caudad and 11 orad. The mean period of colonic migrating myoelectric complexes was 52.7 +/- 6.5 (SE) min. We conclude that the characteristics of colonic migrating myoelectric complexes are strikingly different from those of migrating myoelectric complexes in the small intestine.
Animals↗
Effect of xylazine, cisapride, and naloxone on myoelectric activity of the ileocecocolic area in cows.
The effect of xylazine, cisapride, and naloxone on myoelectric activity of the ileum, cecum, and proximal loop of the ascending colon (PLAC) was determined in 4 healthy Jersey cows implanted with 8 pairs of bipolar electrodes. A 4 x 4 Latin square design was used. The treatments included xylazine (0.04 mg/kg of body weight), cisapride (0.08 mg/kg), naloxone (0.05 mg/kg), and 0.9% sodium chloride solution (20 ml). All treatments were administered i.v. during early phase I of the migrating myoelectric complex in the ileum. Myoelectric activity was recorded for 4 hours after treatment, and data were analyzed for each hour separately. Xylazine significantly (P < 0.05) increased the duration of phase I of the first migrating myoelectric complex in the ileum to 220.72 +/- 26.89 minutes, compared with 30.91 +/- 10.11 minutes after administration of 0.9% sodium chloride solution. The number of cecocolic spikes per minute per electrode and the duration of cecocolic spike activity (percentage of recording time) were significantly (P < 0.05) decreased for the first 3 hours, and the number of propagated spike sequences in the cecum and PLAC was significantly (P < 0.05) decreased for the first 2 hours after administration of xylazine. Significant difference was not found between control and either cisapride or naloxone treatment of healthy cows. However, during hour 1 after treatment with cisapride, number of spikes per minute, duration of spike activity, and number of propagated spike sequences were highest, compared with the other treatments.(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
Effect of total sympathectomy and of decentralization on migrating complexes in dogs.
The effect of total sympathectomy and of decentralization on interdigestive myoelectric activity of the stomach and small intestine and on cycling levels of plasma motilin were studied in conscious dogs. In controls, 98.3% +/- 7.9% of the migrating myoelectric complexes (mean +/- SD) originated in the stomach. In sympathectomized dogs, 38.17% +/- 16.7% originated in the stomach, 35.8% +/- 12.3% in the duodenum, and 26.3% +/- 4.3% in the jejunum. In decentralized dogs, 5.3% +/- 1.4% of the migrating myoelectric complexes originated in the stomach, 71.0% +/- 16.5% in the duodenum, and 23.9% +/- 17.4% in the jejunum. Cycling of plasma motilin was not affected by long-term sympathectomy but coordination of peak levels of plasma motilin and initiation of gastric migrating myoelectric complexes was disrupted in decentralized dogs. These data suggest that central nervous input is required for initiation of migrating myoelectric complexes in the stomach and that central vagal but not central sympathectic input is essential for cycling of plasma motilin.
Animals↗
Dopamine-induced migrating myoelectrical complex-like activity in human duodenum.
The effect of dopamine on human gastric and small intestinal interdigestive motility was investigated in 12 subjects. Intestinal motility was recorded by means of a four-lumen polyvinyl probe with four open tips located 15 cm apart, continuously perfused with distilled water. In each subject during the same study, after recording two consecutive spontaneous phase III of migrating myoelectrical complexes and when a phase II appeared, dopamine was infused intravenously twice in a dose of 5 micrograms/kg/min for 15 min with an interval of 20 min between each infusion. In six subjects, the second dopamine infusion was preceded by a treatment with sulpiride (10 mg, intravenously, as bolus) or domperidone (10 mg, intravenously, as bolus), each considered a highly selective dopamine antagonist. The results show that dopamine stimulates duodenal motility producing a pattern similar to that observed in phase III of spontaneously occurring migrating myoelectrical complexes. The second dopamine infusion reproduced in all cases the same pattern of motility as observed during the first infusion. Sulpiride and domperidone prevented the effect of dopamine in all cases. It is therefore suggested that dopamine-induced duodenal motility may involve specific dopaminergic receptors.
Adult↗
Rhythmic oscillating complex: characterization, induction, and relationship to MMC in chickens.
Migrating myoelectrical complexes (MMCs) and rhythmic oscillating complexes (ROCs) have been investigated in chickens prepared for electromyography. Animals were chronically implanted with electrodes in stomach, duodenum, jejunum, ileum, ceca, and rectum. MMCs showing phases I-III were found in the jejunum and ileum both in fed and fasted states. Repetitive spike bursts were recorded in the duodenum (0.5-1/h), disrupting the gastroduodenal coordination and preceding a phase III in the jejunum. ROCs appeared spontaneously in fasted animals and in 75% of the recordings during the dark period. Four consecutive intestinal myoelectrical patterns have been described during a ROC. Briefly, they consisted in series of high-speed propagated abroad contractions of great amplitude that progressively changed into others of orad direction. In relation to the MMC, the ROC pattern appeared just after a phase III reached the distal ileum, and a pattern of duodenal repetitive spike bursts, followed by a migrating phase III in the jejunum, started at the duodenum after a ROC. No myoelectrical changes were recorded in cecorectal activity during ROC. Vagotomized animals showed the ROC pattern. Neither apomorphine (5-100 micrograms/kg iv) nor cholecystokinin (10(-9) mol/kg iv) induced ROCs. Naloxone (5 x 10(-7) mol/kg iv) and atropine (0.1 mg/kg iv) induced isolated orad contractions. Myoelectrical and functional similarities can be found between retrograde giant contractions, described in mammals, and ROCs. However, they differ in their origin and mechanism of induction.
Animals↗
Role of serotonin in the recovery of electrical activity in the stomach and small intestine of rats during the early postsurgery period.
The effects of serotonin and 5-HT4 receptor agonist cisapride on electrical activity of the stomach and small intestine were studied in rats with postoperative ileus. Postoperative ileus was accompanied by the absence of the migrating myoelectric complex in the stomach and small intestine. All phases of the migrating myoelectric complex were successively recovered in the jejunum, duodenum, and stomach. Administration of serotonin and 5-HT4 receptor agonist cisapride into the jejunum was followed by the appearance of spike activity, which spread from the stomach to the jejunum. Intraintestinal treatment with cisapride and serotonin shortened the period to recovery of the migrating myoelectric complex to 3 and 4 days, respectively. Our results suggest that serotonin plays a role in the regulation of the migrating myoelectric complex at the early postoperation period.
Action Potentials↗
Effects of neuropeptide FF on intestinal motility and temperature changes induced by endotoxin and platelet-activating factor.
Several effects of bacterial endotoxins involve an opioid pathway and neuropeptide FF is an endogenous peptide known to modulate opioid activity, mainly in the central nervous system. The aim of this study was to investigate in rats the role of central neuropeptide FF receptors in intestinal motor disturbances and body temperature changes induced by endotoxins and platelet-activating factor (PAF), a major endotoxin mediator. Rats were fitted with intestinal electrodes, an intraperitoneal thermistor probe and an intracerebroventricular (i.c.v.) cannula for long-term use. E. coli endotoxin (100 microg/kg, i.v.) disrupted the cyclic pattern of intestinal migrating myoelectric complexes and induced a biphasic increase in body temperature while PAF (25 microg/kg, i.p.) disrupted the migrating myoelectric complexes and induced hypothermia for about 2 h. The neuropeptide FF analog, (1 DME)Y8Fa (D-Tyr-D-Leu[N-Me]-Phe-Gln-Pro-Gln-Arg-Phe-NH2) administered i.c.v. 40 and 100 microg/kg reduced the duration of migrating myoelectric complex disruption induced by endotoxin and PAF and abolished the PAF-induced hypothermia. Only at the dose of 100 microg/kg did (1 DME)Y8Fa change the biphasic endotoxin-induced hyperthermia into a monophasic increase. Naloxone (1 mg/kg, s.c.) reduced only the duration of migrating myoelectric complex disruption induced by endotoxin. These results indicate that central neuropeptide FF modulates the intestinal motor disturbances and changes in body temperature induced by endotoxin and PAF. Its action against endotoxin may involve an anti-opioid pathway whereas its action against PAF does not.
Animals↗
Clonazepam-induced intestinal motor disturbances are linked to central nervous system release of cholecystokinin in rats.
The central and peripheral effects of clonazepam (central benzodiazepine receptor agonist) on intestinal myoelectrical activity and the origin of the effects were evaluated in conscious rats, chronically fitted with Nichrome electrodes implanted on the jejunum and with an intracerebroventricular (i.c.v.) cannula. Administered intraperitoneally (i.p.) in 12-h fasted rats, clonazepam (0.05 to 0.5 mg/kg) dose dependently disrupted jejunal cyclic migrating myoelectric complexes, characterizing the fasted state, which were replaced by a permanent irregular spiking activity, lasting 259 +/- 37 min for clonazepam at the dose of 0.5 mg/kg. This disruption of migrating myoelectric complexes occurred after a delay which increased with increasing clonazepam doses. In contrast, injected i.c.v. at doses from 1 microgram/kg to 1 mg/kg, clonazepam did not alter the migrating myoelectric complexes pattern of the small intestine. Injected i.p., flumazenil (central benzodiazepine receptor antagonist) (1 mg/kg) but not PK 11-195 (peripheral benzodiazepine receptor antagonist) (5 mg/kg) suppressed the effects of i.p. clonazepam (0.1 mg/kg). Administered i.c.v., 10 min prior to clonazepam (0.1 mg/kg i.p.), devazepide (CCKA receptor antagonist) at a dose as low as 10 ng/kg reduced the migrating myoelectric complex disruption induced by clonazepam. L365-260 (CCKB receptor antagonist) administered i.c.v reduced the migrating myoelectric complex disruption at 10-fold higher doses and loxiglumide (CCKA receptor antagonist) injected i.c.v, at 100-fold higher doses. When administered i.p. neither devazepide nor L365-260 affected the duration of migrating myoelectric complex disruption induced by clonazepam (0.1 mg/kg i.p.) or its delay of occurrence at doses lower than 0.1 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effect of berberine on myoelectric activity and transit of the small intestine in rats.
The motility of the small intestine in unanesthetized rats receiving berberine sulfate (0.2, 2.0, and 20.0 mg/kg i.p.) was investigated. Motility was determined by two methods: myoelectric activity was monitored with indwelling bipolar electrodes, and intestinal transit was measured by the movement of radiochromium (Na51CrO4). The 20.0-mg/kg dose caused a marked inhibition of spike activity for 21.8 +/- 7.0 min and disrupted activity fronts of the migrating myoelectric complex for 212.3 min. Berberine, 2.0 mg/kg i.p., disrupted migrating myoelectric complexes for 64.6 min but spike inhibition was not observed. Transit of the small intestine was significantly (p less than 0.001) delayed at 15 and 100 min after the highest dose of berberine. Naloxone blocked the spike inhibition noted with 20.0 mg/kg of berberine but failed to improve transit. Phentolamine blocked spike inhibition and was associated with a significantly earlier return of activity fronts of the migrating myoelectric complex. Animals pretreated with this antagonist tended toward a higher geometric center in transit studies than those injected with berberine alone. Berberine was also administered by various routes (intraperitoneal injection, intravenous injection, orogastric gavage, and intraluminal injection). An intraperitoneal injection was 10-fold more potent than an intravenous injection. Orogastric gavage and intraluminal administration of berberine did not alter intestinal motility. In summary, berberine sulfate significantly inhibits myoelectric activity and transit of the small intestine. This appears to be partially mediated by opioid and alpha-adrenergic receptors. The antidiarrheal properties of berberine may be mediated, at least in part, by its ability to delay small intestinal transit.
Administration, Oral↗
Muscarinic cholinergic receptor density following small intestinal transplantation in rats.
After small intestinal transplantation, intestinal isografts can organize migrating myoelectric complexes, and we have shown that migrating myoelectric complex frequency in the fasted state was reduced compared with controls after transplantation of the distal 50% of small intestine. We hypothesized that changes in motor activity after transplantation were related to alteration of cholinergic nerve activity or receptor density. With use of standard microsurgical techniques, the distal 50% of small intestine was orthotopically transplanted in a Lewis-to-Lewis donor-recipient combination. Resection controls were prepared by resecting the proximal 50% of small intestine, and sham controls were prepared by performing a sham laparotomy. Two months after surgery, small intestine was harvested. Choline acetyltransferase activity among the three groups was similar, suggesting that intrinsic cholinergic nerves remained intact. There was a strong trend toward decreased acetylcholinesterase activity [analysis of variance (ANOVA), P = 0.16] after transplantation, consistent with loss of extrinsic vagal nerve fibers. There were no differences in histochemical distribution of acetylcholinesterase among these groups. Muscarinic receptor density, as determined by binding to [N-methyl-3H]scopolamine, was decreased after transplantation (ANOVA, P = 0.02). There was a trend toward decreased receptor density in animals with resected small intestine. Surgical interruption of intrinsic nerve pathways rather than ischemia or extrinsic denervation might be the mechanism for diminished receptor density after transplantation, and reduced small bowel motor activity may be related to decreased density of muscarinic cholinergic receptors.
Acetylcholine↗
Role of free radicals and platelet-activating factor in the genesis of intestinal motor disturbances induced by Escherichia coli endotoxins in rats.
The effects of IV administration of Escherichia coli endotoxin on intestinal myoelectric activity was investigated in conscious fasted rats chronically implanted with nichrome electrodes in the duodenojejunum. These effects were compared with those of platelet-activating factor and were evaluated in animals pretreated with a specific platelet-activating factor antagonist, BN 52021, indomethacin, a selective prostaglandin E2 antagonist, SC 19220, and several free radical scavengers. Intravenous administration of endotoxin (E. coli S.O111:B4) at a dose of 50 micrograms/kg suppressed the migrating myoelectric complexes, which were replaced by continuous rhythmic clusters of rapidly propagated spike bursts for 114.7 +/- 19.9 minutes. Intraperitoneal platelet-activating factor (25 micrograms/kg) also inhibited the migrating myoelectric complex pattern for 146.1 +/- 24.1 minutes. Previous IV administration of BN 52021 (50 mg/kg-1) abolished the motor alterations induced by platelet-activating factor and significantly reduced to 43.1 +/- 12.2 minutes those induced by endotoxin (P less than 0.01). Indomethacin (10 mg/kg IP), injected before endotoxin or platelet-activating factor, also significantly reduced the duration of migrating myoelectric complex inhibition to 45.6 +/- 7.8 and 47.7 +/- 8.3 minutes, respectively (P less than 0.01). SC 19220 significantly reduced the effects of platelet-activating factor from 151.8 +/- 26.4 to 67.4 +/- 14.7 min (P less than 0.01). Superoxide dismutase (15,000 U/kg IV) injected before either endotoxin or platelet-activating factor shortened the migrating myoelectric complex inhibition to 45.7 +/- 9.9 and 72.9 +/- 10.4 minutes, respectively (P less than 0.01). Allopurinol and dimethylsulfoxide administered orally at 50 mg/kg 1 hour before endotoxin reduced the migrating myoelectric complex inhibition to 42.5 +/- 6.5 and 38.2 +/- 6.4 minutes, respectively (P less than 0.01). They also reduced platelet-activating factor-induced intestinal myoelectric alterations to 68.5 +/- 10.6 and 31.7 +/- 6.1 minutes, respectively (P less than 0.01). It is concluded that endogenous release of platelet-activating factor is partly responsible for the intestinal motor alterations induced by endotoxin, these effects being also mediated through the release of prostaglandins and free radicals. However, prostaglandins, as well as free radicals, appear to be partly involved in the platelet-activating factor-induced action of E. coli endotoxin on intestinal motility.
Animals↗
Estimation of gastric residence time of the Heidelberg capsule in humans: effect of varying food composition.
In animal and human studies, the gastric emptying of large (greater than 1 mm) indigestible solids is due to the activity of the interdigestive migrating myoelectric complex. The gastric residence time (GRT) of an orally administered, nondigestible, pH-sensitive, radiotelemetric device (Heidelberg capsule) was evaluated in three studies in healthy volunteers. In 6 subjects, the GRT of the Heidelberg capsule was compared with the half-emptying time (t1/2) of diethylenetriaminepentaacetic acid labeled with technetium 99m after a 4-ml/kg liquid fatty meal. The mean (+/-SD) GRT (4.3 +/- 1.4 h) was significantly (p less than 0.001) longer than the mean t1/2 (1.1 +/- 0.3 h); the GRT was prolonged compared with the t1/2 in each subject. In a randomized, crossover trial in 10 subjects, frequent feeding caused a dramatic prolongation in mean GRT of the capsule compared with the fasting state (greater than 14.5 vs. 0.5 h, p less than 0.005). In another crossover study in 6 subjects, the GRT of the capsule was evaluated after an overnight fast, a standard breakfast including solid food, and a liquid meal (i.e., 200 ml of diluted light cream). The mean GRT was 2.6 +/- 0.9 h after the liquid meal vs. 1.2 +/- 0.8 h after fasting (p less than 0.025). The mean GRT after the breakfast was 4.8 +/- 1.5 h, which was significantly greater than that after fasting (p less than 0.001) and after the liquid meal (p less than 0.01). These data suggest that the GRT of the Heidelberg capsule is a marker of the interdigestive migrating myoelectric complex in humans, the interdigestive migrating myoelectric complex can be markedly delayed by frequent feedings with solids, and the interdigestive migrating myoelectric complex is delayed by both liquid and solid meals.
Adult↗
A new method for correlating pancreatic and biliary duct pressures and sphincter of Oddi electromyography.
Myoelectric activity of the sphincter of Oddi and duodenum was correlated with pancreatic and biliary duct pressures in eight opossums, in both the fasted and fed states. Four bipolar electrode pairs were implanted in the sphincter of Oddi and duodenum. A polyethylene T tube was placed in the pancreatic duct. The common duct was cannulated through a small bile duct. This method allowed pressure recording for several weeks and avoided interference with the flow of bile or pancreatic juice into the duodenum. The frequency of slow waves was the same in the sphincter of Oddi and duodenum (19 per minute). The variation in the frequency of spike potentials in the sphincter of Oddi correlated to that of the migrating myoelectric complex in the duodenum. The average frequency of slow waves that have superimposed spike potentials in the sphincter of Oddi and duodenum was 3.0 and 0 in phase 1, 4.7, and 6.2 in phase II, 6.1 and 15.1 in phase III, and 3.4 and 6.3 in phase IV, respectively. The average duration of a migrating myoelectric complex cycle was 92 minutes. After feeding, the interdigestive phases of the migrating myoelectric complex were abolished and substituted by a feeding activity pattern that was characterized by an average number of sphincter of Oddi and duodenum spikes of 6.6 and 10.7, respectively. The mean fasting pressure in the pancreatic and biliary duct was 15 and 13 mmHg, respectively. Pressure changes were of two types--synchronous with respiratory movements and with each sphincter of Oddi spike potential. There was no variation in the baseline pressure during the migrating myoelectric complex phases and the fed state. It is concluded that the sphincter of Oddi of the fasting opossum exhibits cyclic changes in the number of spike potentials that correlate with the migrating myoelectric complex in the duodenum. However, the number and amplitude of spike potentials are different in the sphincter of Oddi and duodenum. There is no change in the baseline pressure during fasting and feeding states, and a temporary pressure elevation synchronic with each sphincter of Oddi spike potential was observed.
Action Potentials↗
[Effect of physiological stimuli on Oddi's sphincter motility].
The myoelectric activity of the sphincter of Oddi was studied both in the fasted and fed states and following administration of gastrointestinal hormones. Electromyographic recordings were obtained from 21 opossums in the fasted state and following administration of 20 Cal/kg of fat, protein, carbohydrate or isocaloric mixture of these three aliments. The proximal segment of the sphincter of Oddi generated spontaneous spike potentials that migrated to the distal segment of the sphincter. The frequency of spike potentials correlated with the migrating myoelectric complex in the duodenum. Following feeding, the migrating myoelectric complex was abolished and substituted by a fed pattern. The duration of the fed pattern and the frequency of spike potentials depended on the kind of aliment. Cholecystokinin and pentagastrin increased and glucagon and secretion decreased the frequency of spike potentials in the sphincter of Oddi. It is concluded from these studies that the sphincter of Oddi may play an important role in controlling the time and rate of biliary drainage into the duodenum.
Action Potentials↗
Anamnestic stimulus-specific myoelectric responses associated with intestinal immunity in the rat.
Changes in small intestinal motility reflective of local anaphylaxis are hypothesized to be associated with the rapid, immune-mediated rejection of infective larvae of the nematode Trichinella spiralis. This hypothesis was tested by comparing intestinal myoelectric activity in primarily and secondarily infected rats; the latter group represented immunized hosts, i.e., immunized by initial contact with the parasite. Patterns of slow waves, action potentials, interdigestive migrating myoelectric complexes, and migrating action-potential complexes induced by secondary infection differed from those associated with primary infection. Patterns in both cases differed from those in uninfected rats. Secondary but not primary infection evoked changes in myoelectric patterns within 15 min after administration of infective larvae. These changes could not be elicited by inoculation with dead larvae, larval excretory-secretory antigens, or a heterologous parasite, Eimeria nieschulzi. Results indicate that altered smooth muscle contractile activity is part of an anamnestic, stimulus-specific response to T. spiralis in immunized rats. These changes may represent the in vivo equivalent of the anaphylactically mediated intestinal smooth muscle contraction elicited in vitro in the Schultz-Dale reaction.
Action Potentials↗