SEARCH · PubMed Health

Results for “Myoelectric Complex, Migrating”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources

PubMed2002

Small intestinal transections decrease the occurrence of tapeworm-induced myoelectric patterns in the rat.

Abstract Luminal infection by the noninvasive tapeworm, H. diminuta, alters rat small intestinal myoelectric activity. The significance of continuity between small intestinal enteric nervous system (ENS) and that of both the stomach/pylorus and colon/caecum regarding the induction of tapeworm-altered myoelectric patterns was evaluated. A total of 32 rats were implanted with four serosal electrodes placed at sites in the duodenum through the mid-jejunum. Sixteen of the 32 rats underwent intestinal transections and anastomoses at both the duodenum and ileum. After recording myoelectrical activity of both normal and transected intestines, eight rats from each group (normal and transected) were infected with H.diminuta. Phase III frequency, duration of the migrating myoelectric complex (MMC), slow wave frequency, percentage of slow waves associated with spike potentials and the occurrence of the the two tapeworm-initiated myoelectric patterns, repetitive bursts of action potentials (RBAP) and sustained spike potentials (SSP), were measured. In infected rats, the frequency of the RBAP and SSP electric patterns were significantly reduced by the double transection. Intestinal transection did not affect the other changes caused by infection, such as decreased MMC phase III frequency and percentage of slow waves associated with spike potentials. In conclusion, a small intestinal ENS in continuity with other segments of the GI tract is required to generate maximal numbers of tapeworm-induced SSP and RBAP myoelectric activity in the small intestine of the rat.

Anastomosis, Surgical↗

PubMed1995

Vagal control of fasting somatostatin levels.

UNLABELLED: The relationship between fasting intestinal motility, plasma concentration of somatostatin and vagal integrity was examined in four conscious dogs. Small intestinal motility was recorded using subserosally implanted bipolar electrodes. The cervical vagosympathetic trunks, previously isolated in skin loops, were blocked by cooling. In the fasted state, peaks in somatostatin concentration were observed during phase III of the migrating myoelectric complex (MMC). During vagal blockade, small intestinal MMCs persisted but with phase II being absent or decreased in duration in the duodenum and upper jejunum. Somatostatin levels significantly decreased to below the basal levels observed prior to blockade. No cycling of somatostatin levels was evident during the period of vagal blockade. Upon termination of vagal cooling, normal motility returned and somatostatin levels returned to their pre-blockade levels. IN CONCLUSION: (1) plasma somatostatin levels cycle with phase III of the MMC in the upper small intestine; (2) the cycling of fasting somatostatin concentrations is primarily dependent upon intact vagal pathways; and (3) basal plasma somatostatin levels are in part vagally dependent.

Adaptation, Physiological↗

PubMed1996

Beta-adrenoceptors regulate myoelectric activity in the small intestine of rats: stimulation by beta 2 and inhibition by beta 3 subtypes.

Using beta-adrenergic agonists and antagonists this study investigated the importance of three different adrenoceptor subtypes for the regulation of migrating myoelectric complexes (MMCs) of the upper small intestine in conscious, naive rats. After a control period of 60 min with four activity fronts, agonists were given as an intravenous infusion for another 60 min. The non-selective beta-adrenoceptor agonist isoprenaline (1 microgram kg-1 min-1) inhibited MMCs and induced irregular spiking during the infusion period. This effect was blocked by intravenous administration of a bolus dose of either the non-selective beta-adrenoceptor antagonist propranolol (1 mg kg-1), or the beta 2-antagonist ICI 118 551 (1 mg kg-1), both given prior to isoprenaline. However, acebutolol (1 mg kg-1), a selective beta 1-antagonist, failed to antagonize the effect of isoprenaline. Furthermore, prenalterol, a selective beta 1-agonist (12.5-800.0 micrograms kg-1 min-1), had no effect on the MMC pattern, whereas the beta 2-selective agonist ritodrine (25-100 micrograms kg-1 min-1) induced a myoelectric pattern similar to one induced by isoprenaline. The partial beta 3-adrenoceptor agonist D7114 (50-100 micrograms kg-1 min-1), disrupted the MMCs and induced quiescence. Neither of the antagonists, i.e. propranolol (1 mg kg-1), acebutolol (1 mg kg-1) nor ICI 118 551 (1 mg kg-1), given alone induced changes in the MMC pattern. In conclusion, beta 2-adrenoceptors in particular but also beta 3-adrenoceptors seem to be of importance in the regulation of small intestinal motility by disrupting the regular MMC pattern in rats.

Acebutolol↗

PubMed1994

Benzodiazepine-induced intestinal motor disturbances in rats: mediation by omega 2 (BZ2) sites on capsaicin-sensitive afferent neurones.

1. The central and peripheral effects of the omega (benzodiazepine) site ligands, clonazepam, alpidem, zolpidem, triazolam, flumazenil, ethyl beta carboline-3-carboxylate (beta-CCE) and N-methyl beta carboline-3-carboxylate (beta-CCM) on intestinal myoelectrical activity were evaluated in conscious rats, chronically fitted with Nichrome electrodes implanted on the duodenum and jejunum. The localization of the omega (benzodiazepine) receptors involved in these effects was evaluated by use of systemic and perivagal capsaicin treatments. 2. When administered intraperitoneally (i.p.) the omega site inverse agonists beta-CCE and beta-CCM, and the omega site antagonist flumazenil, did not affect the duodeno-jejunal motility. Alpidem and zolpidem, two selective omega 1 site agonists induced an inhibition of migrating myoelectric complexes (MMCs) only at a high dose (5 mg kg-1). In contrast, clonazepam (a mixed omega 1/omega 2 agonist) and triazolam (a preferential omega 2 site agonist) disrupted the MMC-pattern at doses as low as 0.05 mg kg-1, the effect of trizolam being of much longer duration than that of clonazepam. None of these drugs altered MMC-pattern when administered centrally (i.c.v.). 3. Administered i.p. or i.c.v. prior to triazolam, alpidem blocked the effect of triazolam on duodenojejunal spike activity. Administered i.p. prior to triazolam, flumazenil suppressed the triazolam-induced MMC-disruption. Previous systemic but not perivagal capsaicin treatment suppressed the effects of clonazepam on MMCs. 4. It is concluded that omega-site agonists but not, antagonist or inverse agonists, administered systemically induced intestinal motor disturbances which may be linked to activation of omega 2 (BZ2) sites located on nonvagal capsaicin-sensitive afferent neurones.

Animals↗

PubMed1994

Intestinal motility responses to neuropeptide gamma in vitro and in vivo in the rat: comparison with neurokinin 1 and neurokinin 2 receptor agonists.

We have studied the effect of a novel tachykinin, neuropeptide gamma (NP gamma) on small intestinal motility in the rat. Experiments were done in vitro on longitudinal muscle strips of duodenum, and in vivo on the migrating myoelectric complex (MMC) of the small intestine. In vitro, contractile effects of NP gamma were compared with those of a selective neurokinin 1 (NK1) receptor agonist, substance P methyl ester (SPME), and a selective neurokinin 2 (NK2) receptor agonist, Nle10-NKA(4-10)(NleNKA). NP gamma, SPME and NleNKA caused concentration-dependent contractions (P < 0.001). NP gamma was eight-fold more potent than NleNKA, and 118-fold more potent than SPME. Contractile responses to NP gamma were reduced by hexamethonium (P < 0.01) and atropine (P < 0.05). The non-selective NK receptor antagonist spantide I only slightly reduced the contractile response to NP gamma, as did the selective NK1 antagonist GR 82,334, and the selective NK2 antagonist L-659,877 and MEN 10,376. In vivo, effects of NP gamma on the MMC were compared with those of the natural tachykinins substance P (SP) and neurokinin A (NKA). NP gamma disrupted the MMC and induced irregular spiking in a dose-dependent manner from 25 to 100 pmol kg-1 min-1 i.v. (P < 0.05). The effect of NP gamma was more prominent than that of NKA at equal doses, while SP had no effect. Our findings show that NP gamma exerts potent stimulatory effects on small intestinal motility, most likely mediated directly via distinct NK receptors on smooth muscle cells, but also indirectly via a cholinergic link.

Animals↗

PubMedDate not supplied

Myoelectric activity in the intestine of cows with strangulating obstruction of the distal small intestine.

Myoelectric activity in 2 cows instrumented with permanent electrodes in the ileum, cecum, proximal loop of the ascending colon (PLAC), and spiral colon was analyzed after an obstruction developed in the distal small intestine. Results were compared with patterns from a group of 7 normal cows. Myoelectric activity in the ileum immediately orad to the occlusion was characterized by abolition of the migrating myoelectric complex (MMC) and a constant pattern of strong spike bursts of long duration. Cyclic activity was present in all parts of the large intestine, and propagation of phase III activity was evident from proximal to distal. A slight degree of disorganization in phase III propagation was restricted to the spiral colon. Activity cycles tended to be shorter in the cecum and PLAC of both cows with colic than in normal cows, and the intensity of spiking activity was generally lower. Changes in duration of the MMC in the spiral colon (bovine colonic MMC, bcMMC) were inconsistent, but the intensity of spiking activity tended to be lower in phases I and II of both cows compared to controls. The organization of phase III in several spindles typical of the bovine spiral colon was not disrupted, but phase IV of the bcMMC occurred only infrequently. Organized cyclic activity occurred in the large intestine of both cows despite complete disruption of the small intestinal MMC, indicating the presence of mechanisms able to initiate and regulate coordinated myoelectric patterns in the large intestine independent of the small intestine.

Animals↗

PubMed1995

Effect of neural blockades, gastrointestinal regulatory peptides, and diversion of gastroduodenal contents on periodic pancreatic secretion in the preruminant calf.

The role of nerves, gastrointestinal peptides, and gastroduodenal contents in the regulation of pancreatic periodic function were studied in preruminant calves. Nine male, Friesian calves were surgically fitted with pancreatic and duodenal catheters, abomasal and duodenal cannulae, and duodenal electrodes. Pancreatic secretion oscillated in phase with the duodenal migrating myoelectric complex. Pancreatic secretion and duodenal motility were abolished by intravenous atropine (5 micrograms.kg-1.min-1). The frequency of pancreatic and duodenal cycles was similarly increased by motilin and decreased by pituitary adenylate cyclase activating polypeptide-27; secretin lengthened duodenal but not pancreatic cycles, resulting in loss of synchronization; cholecystokinin-8 and secretin increased pancreatic secretion (all infusions at 120 pmol.kg-1.h-1); intraduodenal lidocaine (2%) or diversion of gastroduodenal contents reduced pancreatic secretion without altering periodicity. In conclusion, generation of pancreatic as well as of duodenal periodicity in the calf depends upon cholinergic neural efferent input. Secretin, cholecystokinin-8, pituitary adenylate cyclase activating polypeptide, duodenal contents, and mucosal afferent receptors seem to have relatively minor regulatory roles but can modulate the level of pancreatic secretion. The importance of enteric neural influence from the duodenum and the role of motilin in the regulation of pancreatic periodicity and its synchronization with the duodenal motility cycle remain to be determined.

Anesthetics, Local↗

PubMed1991

Intestinal motility changes in rats after enteric serotonergic neuron destruction.

The myenteric plexus consists of several subpopulations of morphologically and chemically distinct neurons known to contain a variety of peptides and amines, one of which is serotonin (5-hydroxytryptamine). These neurons are considered essential for nerve-to-nerve transmission. In the present study, we investigated the effect of 5,6- and 5,7-dihydroxytryptamine (5,6-DHT; 5,7-DHT), indoleamine neurotoxins that selectively and irreversibly injure the serotonergic neurons of the myenteric plexus. Treatment with 5,6-, or 5,7-DHT caused marked disruption of the activity front of the migrating myoelectric complex (MMC), increased its duration, and decreased its propagation velocity. At higher doses, 5,7-DHT also reduced the slow-wave frequency. Immunohistochemical techniques showed that tissue from rats treated with 5,7-DHT was depleted of serotonin-like immunoreactivity within the myenteric plexus neurons. Reserpine also caused motility and immunohistochemical changes similar to those induced by the two neurotoxins. Therefore, destruction of enteric serotonergic neurons disrupts the MMC. These studies support the cellular concepts that serotonergic neurons function as interneurons in the myenteric plexus, modulating and processing the neural stimuli, and that serotonin is an important neurotransmitter in the small intestine.

5,6-Dihydroxytryptamine↗

PubMed1992

Leuprolide acetate affects intestinal motility in female rats before and after ovariectomy.

Leuprolide acetate, a gonadotropin-releasing hormone (GnRH) analogue, is currently being proposed to control debilitating symptoms in women with functional bowel disease. Whether leuprolide alters gastrointestinal motility as part of its actions is unknown. This study was designed to assess, using myoelectric techniques in an animal model, the effects of leuprolide on potential mechanisms of neuromuscular function of small intestine. Female rats with (n = 6) or without (n = 8) bilateral ovariectomy were used to study jejunal motility before and after leuprolide therapy. Throughout the study, daily leuprolide dosages of 0.02, 0.2, or 0.4 micrograms/kg were injected into intact rats and 0.02, 0.2, 0.4, 1.0, or 2.5 micrograms/kg into ovariectomized rats. Recordings were made while the rats were fasted and postprandial and before and after leuprolide administration. Under control conditions, migrating myoelectric complexes (MMCs) were found in intact female rats, whether fasted or postprandial. After ovariectomy, postprandial controls and those treated with low-dose leuprolide (0.02, 0.2, and 0.4 micrograms) had typical fed-state patterns and no MMCs, but at 1.0 and 2.5 micrograms the fed state was inhibited and cycling MMCs occurred at a frequency similar to that of fasted controls. Reproductive hormones thus have a significant effect on gastrointestinal motility.

Animals↗

PubMed1992

Intestinal myoelectrical activity and transit time in chronic portal hypertension.

This study was designed to determine the effects of portal hypertension on intestinal myoelectrical activity and propulsion. In a single surgery, adult rats were implanted with a serosal electrode at each quarter of the small intestine, and portal hypertension was produced by calibrated constriction of the portal vein. To determine intestinal transit, portal vein-stenosed (PVS) and sham-operated animals were chronically implanted with a catheter in the proximal small intestine. Transit time was determined by measuring the progression of radioactive chromium along the bowel. Studies were conducted 6, 9, and 14 days after surgical preparation. Portal hypertension was associated with both transient and persistent changes in intestinal myoelectrical activity during the experimental period. Slow wave frequency was significantly reduced in the proximal small intestine on all test days and in the distal small intestine on day 14. Occurrence of the migrating myoelectric complex was reduced on days 6 and 9. Phase III amplitude was significantly reduced in the distal small intestine on all test days. Changes in intestinal myoelectrical activity in PVS animals were not associated with measurable changes in intestinal propulsion. The results suggest that both transient and persistent changes in intestinal myoelectrical activity occur during the 2-wk period after portal vein stenosis. The functional significance of the changes is unknown.

Action Potentials↗

PubMed1992

Biomechanical properties of duodenal wall and duodenal tone during phase I and phase II of the MMC.

We used a new method, impedance planimetry, to look at variations in compliance, tone, and distension-induced peristaltic activity during phase I and phase II of the migrating myoelectric complex (MMC) in the human duodenum. A balloon was inflated stepwise with pressures up to 30 cmH2O in the duodenum, while the pressure and balloon cross-sectional area (CSA) were measured simultaneously. The biomechanical wall parameters were calculated from these measurements. Nine duodenal phase IIIs were recorded in six subjects. A balloon pressure of 20 cmH2O induced a smaller CSA in early phase I [266 (236-324) mm2] than in late phase II [385 (276-474) mm2] (P < 0.05). Balloon distensions elicited no contractions in phase I, whereas they increased contractile activity 60% (P < 0.05) proximal to the balloon and 4% distal to the balloon in late phase II. Step distensions in phase I with balloon pressures between 10 and 30 cmH2O increased the CSA from 40 (30-81) to 645 (603-704) mm2. It increased circumferential wall tension from 35 (28-63) to 429 (402-466) mm x cmH2O and the pressure elastic modulus from 9.7 (9.0-14.7) to 33.8 (27.6-33.8) cmH2O, respectively. Thus compliance differs from phase I to phase II. This is most likely caused by increased smooth muscle tone during phase I. Duodenal wall stiffness increases with the balloon pressure applied.

Adult↗

PubMed1994

Intestinal myoelectric alterations in rats chronically infected with the tapeworm Hymenolepis diminuta.

This study determined that intestinal myoelectric activity was profoundly altered during a strictly luminal, chronic, tapeworm infection. Chronically implanted bipolar electrodes were attached to five sites on the serosal surface of the rat small intestine. One was placed on the duodenum, three on the jejunum, and the fifth on the ileum. Electromyographic recording in nonfasted unanesthetized animals was begun at day 5 postsurgery. All electromyographic recordings were analyzed for slow wave (SW) frequency, phase III frequency, duration of phase III, and percentage of SW with spike potentials. Three initial control recordings prior to infection confirmed the presence of normal interdigestive motility characterized by the three phases (I, II, III) of the migrating myoelectric complex (MMC). Two nonpropulsive myoelectric alterations were observed in infected animals: the repetitive bursts of action potentials (RBAP) and periods of sustained spike potentials (SSP). Myoelectric activity from infected animals indicated decreased cycling of the interdigestive MMC. RBAP and SSP were more prevalent in the distal small intestine corresponding to tapeworm location. The percent of spike potential activity indicated that there was a reversal in the spike potential gradient on the small intestine. The number of spike potentials was maximal in caudal and minimal in oral intestine. We propose that overall localized increases in myoelectric spike potential activity represent increased contractility and decreased propulsion triggered by the presence of the tapeworm. These motility changes were surprising, since the tapeworm Hymenolepis diminuta does not penetrate the intestinal mucosa. This interaction between parasite and host may prevent expulsion of the tapeworm from the small intestine.

Action Potentials↗

PubMed1994

Induction of postprandial intestinal motility and release of cholecystokinin by polyamines in rats.

Polyamines are known to play a major role in postprandial adaptation of the digestive tract. Experiments were designed to determine whether ingested polyamines induce change in intestinal motility associated with a cholecystokinin (CCK) release and whether endogenous polyamines are involved in the intestinal and colonic motor response to a meal. Intestinal and colonic motility was assessed in rats equipped with intestinal electrodes, and plasma CCK was determined using a bioassay. Orogastric administration of putrescine, spermidine, or spermine (20 mumol) disrupted intestinal migrating myoelectric complexes (MMCs) and increased the frequency of colonic spike bursts. After a 6-day treatment with the ornithine decarboxylase inhibitor alpha-difluoromethylornithine, the duration of postprandial disruption of MMCs, but not the stimulation of colonic motility, induced by a 3-g meal was significantly reduced. The duration of MMC disruption and the increase in colonic spike burst frequency after spermidine administration (20 mumol) were significantly reduced by CCK-A and CCK-B antagonists. Eight minutes after saline administration plasma CCK concentration was 0.9 +/- 0.4 pM; it rose to 4.7 +/- 2.8 pM, 8 min after spermidine (20 mumol). These results indicate that exogenous polyamines disrupt intestinal MMCs and stimulate colonic motility through a release of CCK acting at CCK-A and CCK-B receptors and suggest that endogenous polyamines are involved in the postprandial control of intestinal motility.

Animals↗

PubMed1995

Duodenal pH governs interdigestive motility in humans.

In this study, we examined the potential influence of duodenal pH in regulating the occurrence of the interdigestive migrating myoelectric complex (IMMC). Fasting gastroduodenal motility, duodenal pH, and plasma motilin were studied in 15 healthy subjects. During phase I, duodenal pH remained stable at 7 +/- 0.2. Phase II was accompanied by a lowering of duodenal pH, which fluctuated between 2.0 and 7.5. During late phase II, the duodenal pH increased to 6.9 +/- 0.3 and remained in the alkaline range during phase III. In six of 46 episodes of the IMMC, the occurrence of gastric phase III was delayed. This was associated with a persistently low duodenal pH (< 4) during late phase II. Despite a normal cyclic increase of plasma motilin, no gastric phase III activity was observed until the duodenal pH exceeded 7.0. Further studies showed that lowering of duodenal pH by intraduodenal perfusion of HCl prevented the occurrence of gastric phase III. We concluded that regularity of IMMC is governed by duodenal pH. An alkaline pH is essential for the initiation of gastric phase III; lowering of duodenal pH prevents its occurrence despite normal cyclic increase of plasma motilin.

Adolescent↗

PubMed1998

Effect of cerebroventricular perfusion of bombesin on gastrointestinal myoelectric activity.

The effect of intracerebroventricular (i.c.v.) perfusion of bombesin (BBS) on the interdigestive migrating myoelectric complex (MMC) activity was examined in conscious dogs with electrodes implanted on the stomach and small intestine. Cannulas and a catheter were chronically positioned in the lateral and fourth cerebral ventricles, respectively. i.c.v. perfusion of BBS, which failed to increase plasma BBS levels, replaced phase I activity in the stomach and duodenum by intense irregular spike activity and decreased the occurrence rate of MMCs, whereas intravenous infusion of BBS evoked phase II-like activity, mainly in the jejunum and ileum, and suppressed phase III activity. These data suggest that the effect of i.c.v. administration of BBS was mediated by direct activation of central brain structures. During i.c.v. perfusion of BBS, cycling in plasma levels of motilin persisted even when phase III activity was absent and plasma levels of epinephrine rose significantly. Epinephrine infusion, however, did not affect myoelectric gastrointestinal activity except for prolonging phase II. Thus it is unlikely that the central action of BBS is exerted by motilin or epinephrine.

Animals↗

PubMed1994

Long-term perfusion of the cerebroventricular system of dogs without leakage to the peripheral circulation.

Methods developed previously for studying the effect of cerebroventricular injection or ventriculocisternal perfusion of test substances are unsatisfactory because the test substance is not confined to the central compartment. Most likely the test substance enters the peripheral circulation via the arachnoid villi. The purpose of this paper is to describe a method for perfusing the cerebroventricular system of conscious dogs without passage of test substances to the peripheral circulation. With the method described, the mean (+/- SE) cerebroventricular pressure in conscious dogs was 7.4 +/- 0.8 cmH2O (n = 16), and the mean (+/- SE) production of cerebrospinal fluid (CSF) was 25 +/- 0.3 microliter/min (n = 16). Endogenously occurring migrating myoelectric complexes (MMCs) of the small intestine were recorded in dogs before catheters were implanted in the left and right lateral ventricles and the fourth ventricle and after catheter implantation during cerebroventricular perfusion with artificial CSF alone or with CSF containing sulfated (S-CCK-OP) or nonsulfated cholecystokinin octapeptide (NS-CCK-OP). Only cerebroventricular perfusion with S-CCK-OP (1.2 pmol.kg-1.min-1; n = 20) replaced spontaneously occurring MMCs with a fed-like pattern of myoelectric activity. The results suggest that replacement of the fasting pattern of myoelectric activity with a fed-like pattern in the fasted dog was mediated by CCK-A receptors located in one or more brain nuclei surrounding the third ventricle.

Animals↗

PubMed1995

Intraluminal lipids modulate avian gastrointestinal motility.

Infusion of lipids into the ileum delays gastric emptying and intestinal transit time in some species. The aim of this study was to characterize the actions of intraluminal lipid infusion on gastrointestinal electrical activity in chickens. Animals were prepared for electromyography with chronic electrodes in stomach, duodenum, and small intestine. Two catheters were chronically placed in the esophagus and ileum to infuse equimolar doses of either oleic acid (OA) or triolein (TO). Both OA and TO, esophageally infused, inhibited the frequency of the gastroduodenal cycle and increased the frequency of antiperistaltic spike bursts in the duodenum. Ileal infusion of OA, but not of TO, produced the same effects. Both esophageal and ileal OA infusion increased the duration of the migrating myoelectric complex (MMC) and decreased the speed of propagation of phase III. In conclusion, intraluminal infusion of lipids modulates gastrointestinal motility by decreasing the frequency of the gastric cycle, increasing duodenogastric refluxes, and elongating the MMC. These actions could delay gastric emptying and increase transit time, which suggests the presence of an "ileal brake" mechanism similar to that described in mammals.

Animals↗

PubMedDate not supplied

Myoelectric activity of an ileal isoperistaltic or antiperistaltic loop interposed between colon and rectum: an experimental study in pigs.

The myoelectric activity of 25-30 cm ileal loops interposed isoperistaltically or antiperistaltically between colon and rectum was investigated 1-3 and 20-22 weeks after surgery, in growing pigs chronically fitted with intraparietal electrodes on the loop and the ileum. The fundamental motor profile of the small intestine consisting of migrating myoelectric complexes (MMC) was present on both loops; the MMCs were propagated on the antiperistaltic loop in the original anatomical direction. There was no coordination between the occurrence of phase 3 on the loop and the ileum. Some minor differences concerning the duration, the frequency and the velocity of propagation of phase 3 were observed between the loops and the ileum. Moreover propagated clusters of spike bursts and propagated long duration spike bursts appeared on the isoperistaltic and antiperistaltic loop, respectively, but not on the ileum. No prominent differences in the motor profiles of the loops have been observed between 1-3 and 20-22 weeks after surgery. It is concluded that despite the presence of semisolid contents with an abundant microflora the fundamental intestinal motor profile persists in ileal loops interposed between colon and rectum.

Animals↗