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PubMed1987

Vincristine alters myoelectric activity and transit of the small intestine in rats.

We investigated the motility of the small intestine in unanesthetized rats receiving vincristine (0.075, 0.50, 0.75 mg/kg i.v.). 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). Only the animals injected with the two higher doses had two distinct patterns of altered intestinal myoelectric activity within 2 h of drug administration. The first alteration occurred 44 +/- 6 min after vincristine administration and consisted of a marked increase in action potential activity with disruption of the migrating myoelectric complex. The second alteration consisted of a reappearance of the activity front of the migrating myoelectric complex with a significantly shorter periodicity. A marked reduction in spike activity occurred 3 days after vincristine injection in 3 of 10 animals receiving vincristine. A biphasic response was noted in intestinal transit. Disrupted activity front formation was associated with a significant delay in small bowel transit. In contrast, frequent activity front formation in rats was associated with significantly hastened transit. In summary, vincristine administration induces alterations of myoelectric activity of the small intestine in fasted rats and is associated with changes in intestinal transit.

Action Potentials↗

PubMed1986

Effect of 16,16-dimethyl prostaglandin E2 on the myoelectric activity of the gastrointestinal tract of the opossum.

Myoelectric recordings of the opossum gastrointestinal tract were performed during continuous infusion of 16,16-dimethyl prostaglandin E2 at 0.1, 1, 2 and 5 micrograms/kg X h. Continuous administration of prostaglandin caused a dose-dependent reduction of the duration of the migrating myoelectric complex cycle and an increase in the velocity of phase III migration from the duodenum to the terminal ileum. The reduction of the migrating myoelectric complex cycle was due to a shortening of the duration of both phase I and II. Bolus administration of 16,16-dimethyl prostaglandin E2 caused intense spike activity for 2-4 min in all recording sites simultaneously. Administration of indomethacin did not change the myoelectric activity of the gastrointestinal tract. Infusion of prostaglandin E2 caused diarrhoea in eight of forty experiments. These changes in gastrointestinal motility may be important contributory factors in the pathogenesis of prostaglandin-induced diarrhoea.

16,16-Dimethylprostaglandin E2↗

PubMed1984

Trichinella spiralis: intestinal myoelectric activity during enteric infection in the rat.

The objective was to characterize changes in the host's small intestinal smooth muscle contractile activity caused by the enteric stages of the nematode, Trichinella spiralis, during primary infection. Myoelectric activity was recorded from electrodes permanently implanted on the seromuscular surface of the small bowel in conscious, unrestrained rats during the first 2 weeks postinfection (PI). Several myoelectric parameters examined collectively indicated that smooth muscle function of the small bowel was altered by infection. A decrease in contractile activity was indicated by reductions in electrical slow wave and spike potential frequencies that were maximal 6-12 days postinfection. Normal coordinated contractile behavior was also impaired, as evident from a reduction in the frequency of migrating myoelectric complexes. An infection-induced qualitative change occurred designated as a migrating action potential complex. This unusual spiking activity swept down the bowl rapidly, occurred with greatest frequency 2-6 days PI, and coincided with the disruption of the normal migrating myoelectric complex. It is concluded that recordings of intestinal myoelectric activity provide sensitive, quantifiable correlates of contractile patterns throughout the intestinal phase of trichinellosis in a single host.

Action Potentials↗

PubMed1991

Suppression of castor oil-induced diarrhoea by alpha 2-adrenoceptor agonists.

The effects of systemic administration of alpha 2-adrenoceptor agonists on migrating myoelectric complexes and castor oil-induced diarrhoea of the small intestine were studied in conscious rats. Castor oil (1 mg/kg, intraduodenally) disrupted the migrating myoelectric complexes and induced irregular spiking activity with sporadic bursts of myoelectric activity. This change of motility pattern was present concomitant with diarrhoea 1-2 h after instillation of castor oil and during the whole period of diarrhoea. Pre-treatment with clonidine (5-10 micrograms/kg i.v.) or oxymetazoline (5.6-11.2 micrograms/kg i.v.), a peripherally active alpha 2-agonist, inhibited the irregular spiking induced by castor oil and no diarrhoea occurred during the experimental period of 6 h. Thus, the antidiarrhoeal action of peripherally acting alpha 2-adrenoceptor agonists such as oxymetazoline, may be of clinical value in the treatment of diarrhoea.

Adrenergic alpha-Agonists↗

PubMed1975

Electrical activity of the ovine jejunum and changes due to disturbances.

Spike potential activity of the jejunum was recorded from chronically implanted electrodes in conscious sheep. The activity was summed at 20-sec intervals before, during, and after induction of diarrhea, small-bowel obstruction, and after nerve section. Sheep on a normal diet regimen exhibited migrating myoelectric complexes at a frequency of 18/24 hr. These complexes displayed irregular and regular activities which occupied 67% of the recording time. A common pattern observed during the manipulations was disorganization of the motor profile. The normal pattern was replaced by continuous spiking activity followed in many cases by total quiescence. After vagotomy the complexes still occurred but the duration of irregular spiking activity was decreased. These experiments suggest that the migrating myoelectric complex acts as a regulating factor and suggests that the ratio of irregular to regular activity is dependent on the influence of extrinsic nerves.

Animals↗

PubMed1982

Central regulation of intestinal motility by somatostatin and cholecystokinin octapeptide.

When injected continuously into the lateral ventricles of the rat, somatostatin increased the frequency of the migrating myoelectric complexes of the small intestine in a dose-related manner. A significant increase was obtained at a dose as low as 0.066 picomole per minute. In contrast, cholecystokinin octapeptide decreased the frequency of the migrating myoelectric complex of the small intestine or disrupted this pattern when injected into the lateral ventricle at rates of 0.073 to 0.23 picomole per minute. These findings support the hypothesis that somatostatin and cholecystokinin octapeptide act on central nervous system structures that are involved in the control of intestinal motility.

Animals↗

PubMed1984

Influence of transsphincteric fluid flow on spike burst rate of the opossum sphincter of Oddi.

In this study, we evaluated the effect of transsphincteric fluid flow on the rate of spike bursts in the opossum sphincter of Oddi (SO). For chronic studies in awake animals, bipolar electrodes were implanted on the SO, gastric antrum, duodenum, and jejunum. In group 1 animals, surgery was limited to electrode implantation. Subsequently, these animals underwent a cholecystectomy. Group 2 animals had electrode implantation without further surgery. In group 3 animals, bile flow was diverted around the SO, whereas in group 4 animals, pancreatic juice as well as bile was diverted around the SO. Multiple myoelectric recordings were obtained in each animal during fasting and after feeding. In fasted control animals, the rate of SO spike bursts showed cyclic increases synchronous with phase III of the duodenal migratory myoelectric complex. Feeding increased the rate of SO spike bursts. Cholecystectomy had no effect on SO spike bursts in fasted animals. Diversion of bile or bile and pancreatic juice around the SO did not alter the fasting pattern of SO spike bursts. However, flow diversion in the group 3 and group 4 animals did cause a modest decrease of SO spike bursts, from approximately 2/min to about 1/min, during phase I of the duodenal migrating myoelectric complex (p less than 0.05). Sphincter of Oddi spike-burst rate was not affected during the remainder of the migrating myoelectric complex cycle. Neither cholecystectomy nor flow diversion caused any change in the normal SO responses to feeding. Excitatory SO responses caused by motilin or by cholecystokinin-octapeptide were shown to be independent of changes in transsphincteric flow. We conclude that variations in transsphincteric flow cause only minimal alteration of the rate of spike bursts in the opossum SO during fasting. Therefore, factors other than transsphincteric flow, such as hormonal or neural influences, appear to be the major mechanism(s) that regulate the rate of SO contractions in awake opossums.

Action Potentials↗

PubMed1992

Further investigations on the antipropulsive effect of centrally administered histamine and its relation with morphine.

The effect of intracerebroventricularly (i.c.v.) administered histamine (100 micrograms/rat) on intestinal myoelectrical activity was investigated in the jejunum of fasted rats. Histamine caused the disappearance of phase III and a partial reduction of phase II of migrating myoelectric complexes. This effect was antagonized by i.c.v. pretreatment with mepyramine (10 micrograms/rat), an H1 receptor antagonist. Lesions of central noradrenergic neurons by i.c.v. injection of the neurotoxin 6-hydroxydopamine strongly reduced both the inhibition of intestinal propulsion and the migrating myoelectric complexes profile induced by i.c.v. histamine, whereas pretreatment with p-chlorophenylalanine, a selective depletor of serotonin stores, had no effect. It thus appears that aminergic pathways are involved in the visceral effects of central histamine. Mepyramine (200 micrograms/rat i.c.v.) partially reduced the slowing of intestinal transit induced by high doses of morphine. Pretreatment with compound 48/80 (10 micrograms/rat i.c.v.), a mast cell degranulator, but not with alpha-fluoromethylhistidine, an irreversible inhibitor of histidine decarboxylase, reduced the antipropulsive action of i.c.v. morphine to the same extent as mepyramine, suggesting that histamine released from cerebral mast cells by high doses of morphine could contribute to the intestinal inhibition by morphine.

Animals↗

PubMed1993

Periodic fluctuations in pancreatic secretion and duodenal motility investigated in neonatal calves.

To clarify the relative timing of clinical changes in duodenal motility and pancreatic secretion in newborn calves, we recorded duodenal electrical and mechanical activity and analysed pancreatic secretion and migrating myoelectric complex (MMC). In eight calves integrated recordings were derived from sites near the duodenal bulb and pancreatic accessory duct orifice, and pancreatic juice was sampled after an overnight fast, after a feed, and during reversible cold vagal blockade. Peak secretion coincided with duodenal irregular spiking activity and the nadir with absence of spiking. Feeding elicited electrical and mechanical hyperactivity in the duodenum, dissipated the MMC temporarily, and dramatically increased the juice volume and bicarbonate and protein outputs. Periodic fluctuations in secretion started shortly after a feed, as did recovery of the duodenal myoelectric complexes. Cold vagal blockade reversibly disrupted the synchronous changes in duodenal motility and pancreatic secretory activity, though the close association was not totally obliterated. In milk-fed calves interdigestive pancreatic secretion apparently rises and falls in phase with migrating myoelectric complexes of the proximal duodenum and the vagus is largely, though not exclusively, responsible for co-ordinating these changes.

Animals↗

PubMed1989

Migration of the myoelectric complex after interruption of the myenteric plexus: intestinal transection and regeneration of enteric nerves in the guinea pig.

The effects of surgical interruption of the myenteric plexus (myectomy), extrinsic denervation of a length of small intestine, or transection and reanastomosis of the intestinal wall on migration of phase III of the migrating myoelectric complex was studied in guinea pigs. In addition, the recovery of phase III migration and the regrowth of intestinal nerves and muscle across the reanastomosis was studied at various times up to 60 days after surgery. At 6-9 days after surgery, phase III did not migrate past the myectomy during 50%-60% of recorded migrating myoelectric complexes and transection and reanastomosis of the intestinal wall blocked aboral progression of phase III in 90% of cases. Extrinsic denervation did not alter phase III migration through the denervated segment. Phase III migration past the reanastomosis recovered with time after surgery; 80% recovery occurred by 60 days after surgery. Immunoreactivities for vasoactive intestinal peptide, gastrin-releasing peptide, and somatostatin were used as markers for intestinal nerves that were cut by transaction. Immunoreactivities for vasoactive intestinal peptide and gastrin-releasing peptide are contained in myenteric neurons that project in an oral to anal direction to other myenteric ganglia and to the circular muscle. Immunoreactivity for somatostatin is contained in nerve fibers projecting aborally to other myenteric ganglia. At 7-15 days after surgery, there were accumulations of immunoreactivities for vasoactive intestinal peptide, gastrin-releasing peptide, and somatostatin in nerve fibers on the oral side of the reanastomosis, but nerve fibers containing these peptides were not observed in myenteric ganglia or circular muscle close to the anal edge. At 23-28 days, immunoreactivities for vasoactive intestinal peptide, gastrin-releasing peptide, and somatostatin nerve fibers were traced across the reanastomosis and nerve terminals were detected in ganglia and muscle close to the lesion on the anal side. Nerve fibers traversed the lesion in all cases at 57-60 days and vasoactive intestinal peptide-, gastrin-releasing peptide-, and somatostatin-immunoreactive nerve terminals were detected in the first two to three rows of myenteric ganglia on the anal side. Regrowth of intestinal muscle followed a similar time-course to that observed for nerves. These data suggest that interruption of the myenteric plexus alone does not completely block phase III migration. In addition, recovery of phase III migration past a reanastomosis is associated with a restoration of both nervous and mechanical connections.

Animals↗

PubMed1990

Myoelectric activity of the ileum, cecum, and right ventral colon in ponies during interdigestive, nonfeeding, and digestive periods.

Myoelectric activity of the ileum, cecum, and right ventral colon (RVC) was studied in 4 mature ponies. Eight Ag-AgCl bipolar recording electrodes were sutured to the seromuscular layer of the ileum (2 electrodes), cecum (4 electrodes), and RVC (2 electrodes). Myoelectric activity was studied beginning 10 days after surgery. Eight, 60-minute recording sessions were performed in each pony during the interdigestive period, which was the period 3 to 7 hours after the morning feeding. On separate days, food was withheld for 24 hours, and 90-minute recordings were obtained during the nonfeeding period. Ponies were then fed a normal ration, and recordings were continued to obtain data for the digestive (feeding) period. All phases of the migrating myoelectric complex were seen at both ileal electrodes during the interdigestive period, including the periods of no spiking activity (phase 1), irregular spiking activity (phase 2), and regular spiking activity (phase 3). Phase 2 occupied 77% of the total recording time, and the mean duration of phases 1, 2, and 3 was 3.4 +/- 0.2, 12.8 +/- 1.2, and 6.7 +/- 0.7 min, respectively. Frequency of ileal slow waves was 11.8 +/- 0.1/min, and spike burst conduction velocity was 4.7 +/- 0.3 cm/s. A complete migrating myoelectric complex was seen in 11 of 32 tracings (34%) and had a mean duration of 24.2 +/- 2.6 min. The ileal migrating action potential complex, most often seen in phase 2, had a frequency of 4.8 +/- 0.5 spike bursts/h and a conduction velocity of 13.6 +/- 0.4 cm/s.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1988

Effects of experimental duodenal occlusion on electrical activity of the proximal duodenum in cattle.

An electromyographic study of the proximal duodenum in cattle is presented. Changes of motility patterns were studied after induced mechanical obstruction of the descending duodenum in five healthy cows. Special attention was paid to the ratio of antegrade and retrograde motility. Induced duodenal obstruction of which the duration was at most 48 hours, resulted in abrupt disorganisation of the migrating myoelectric complexes; the phases of regular spiking activity disappeared completely or reappeared in a disorganised pattern, and the phases of irregular spiking activity consisted of repetitive groups of spike bursts with prolonged duration and increased propagation velocity. Retrograde peristaltic contractions in the proximal duodenum were observed. Relief of obstruction resulted in a rapid reorganisation of the cyclic pattern of the migrating myoelectric complexes, which indicates normalisation of intestinal activity.

Animals↗

PubMed1985

[Control of antroduodenal motility in sheep].

The continuous but cyclic delivery of contents through the pylorus in the adult ruminant is regulated by the initiation of the migrating myoelectric complexes on the duodenal bulb. The motor responses of the pyloric antrum to the volume of digestive contents, the presence of lipids and ulcerogenic agents revealed that the inhibition of the motor antral activity, whatever its origin, resulted in a higher frequency of the duodenal cyclic motor events. Conversely, stimulation of duodenal motor activity, for example the increased frequency of migrating myoelectric complexes, resulted in the inhibition of the antral motor activity. It is suggested that the motor profile of the antroduodenal junction corresponded to interactions which fulfill the regulation of gastric emptying motor functions, with the first part of the duodenum as an extremely sensitive and rapid controlling mechanism.

Animals↗

PubMed1995

Neurogenic control of myoelectric complexes in the mouse isolated colon.

BACKGROUND/AIMS: Little is known about the mechanisms controlling colonic migrating electrical activity. This study investigates the neural processes involved in the generation of migrating myoelectric complexes in the isolated mouse colon. METHODS: Intracellular electrophysiological recordings were obtained from the circular muscle layer of the mouse colon in vitro in the presence of 2 mumol/L nifedipine. RESULTS: Complexes occurred approximately every 3 minutes and consisted of 1 mumol/L hyoscine-sensitive rapid oscillations (approximately 2 Hz) superimposed on a slow depolarization (approximately 17 mV); the latter was often preceded by a precomplex hyperpolarization (approximately 7 mV) that was reduced by 250 nmol/L apamin. Five hundred micromolars of hexamethonium or 2 mumol/L of tetrodotoxin abolished the complexes and depolarized the muscle by 8.7 +/- 1.3 mV (n = 9) or 12.1 +/- 1.4 mV (n = 5), respectively. Carbachol (50 nmol/L to 5 mumol/L) produced dose-dependent depolarizations but without rapid oscillations. The nitric oxide synthase inhibitor NG-nitro-L-arginine (100 mumol/L) depolarized the tissue by 17.2 +/- 1.6 mV (n = 8) but had no effect on the rapid oscillations. In the presence of 2 mumol/L tetrodotoxin, 5 mumol/L sodium nitroprusside produced a sustained hyperpolarization (15.5 +/- 2.0 mV; n = 5) but did not restore complexes. CONCLUSIONS: In the isolated mouse colon, the membrane potential between complexes is maintained by the release of inhibitory neurotransmitters (including nitric oxide), and the formation of complexes involves disinhibition and the simultaneous activation of cholinergic motor nerves.

Animals↗

PubMed1984

[Intestinal motility following jejunal resection: electromyography study in the rat].

The influences of massive resections on motility of the small intestine remain poorly known. The aim of our study was to determine the effects of jejunal resection on the pattern of occurrence of the migrating myoelectric complex and its postprandial inhibition. The experiments were performed over a period of 1 month after surgery. Transections were done on the jejunum or on the ileum in sham-operated animals. Ten days after resection, the motility of the anastomosed jejunal and ileal segments was dissociated. After one month, a functional continuity appeared through the anastomosis: the whole intestine worked synchronously at the same rhythm as the ileum. Food intake induced an increase in the frequency of the migrating myoelectric complexes measured 10 days after surgery. An adaptative phenomenon appeared after 30 days, the postprandial motor activity returning to its control level.

Animals↗

PubMed1990

Human duodenal myoelectric activity after operation and with pacing.

We sought to determine the influence of operation on the pattern of human duodenal myoelectric activity and to assess whether electrical pacing might correct any postoperative disturbances. Three pairs of temporary bipolar serosal electrodes were placed on the duodenums of ten patients undergoing cholecystectomy. Electrical recordings were obtained daily until the patients' discharge, at 3 to 7 days, after operation. On each postoperative day, a regular rhythmic pattern of pacesetter potentials (PPs) was detected in all patients. The PP frequency (mean +/- SEM) was greater at the proximal electrode than at the distal electrode on the first postoperative day (12.3 +/- 0.1 cpm vs 11.9 +/- 0.1 cpm, p less than 0.01) and on the day of feeding (12.0 +/- 0.2 cpm vs 11.6 +/- 0.2, p less than 0.01). Spontaneous periods when spike potentials accompanied each PP (phase III of the migrating myoelectric complex), were found in only one patient on the day after operation, while they were recorded in five patients after 3 to 7 days, when postoperative ileus had resolved (p less than 0.05). Pacing with electric pulses (50 msec, 5 to 15 mA, 11 to 13 cpm) did not alter the pattern of duodenal PPs or entrain them in the duodenum of any patient at any time after operation. In conclusion, the pattern of duodenal pacesetter potentials changed little during the period of postoperative ileus, while the incidence of phase IIIs of the migrating myoelectric complex was greatly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholecystectomy↗

PubMed1976

Motilin-induced electrical activity in the canine gastrointestinal tract.

Myoelectric activity induced by a synthetic analogue of the duodenal polypeptide motilin, was studied in isolated vascular-perfused canine duodenum and stomach, and in conscious dogs with serosal electrodes implanted in the stomach and the small intestine. In the isolated preparation, the duodenum was found to be four times as sensitive as the antrum to the polypeptide, showing a dose-dependent increase in spike activity within two minutes after administration of the polypeptide. By contrast, in the conscious fasted animal, the only response to motilin, above a threshold dose, was the interpolation of a premature migrating myoelectric complex in the spontaneous interdigestive sequence, appearing fifteen to twenty minutes after the start of infusion. Since the essential difference between the ex vivo and the intact intestine was the preservation of efferent and afferent nervous connections in the latter, it seems that in the conscious animal, the response to exogenous motilin is modulated by the innervation of the intestine, or, alternatively, motilin interacts with the centre controlling the pattern of motor activity in the small intestine rather than directly with smooth muscle. The latter hypothesis is supported by the observation that motilin had no effect on the motor activity of the small intestine during the infusion of pentagastrin which abolishes spontaneous migrating myoelectric complexes.

Action Potentials↗

PubMed1997

Tachykinins influence interdigestive rhythm and contractile strength of human small intestine.

The effect of the putative enteric neurotransmitters neurokinin A and substance P were investigated on human small intestinal motility. Either neurokinin A, at doses of 6-25 pmol/kg/min, or substance P at doses of 1-6 pmol/kg/min were administered intravenously to healthy volunteers over 4 hr. Neurokinin A dose-dependently increased the fraction of phase II of the migrating motor complex, contraction frequency, motility index, and amplitude of contractions. At the highest dose, neurokinin A induced a phase II-like pattern, disrupting the migrating myoelectric complex. Substance P dose-dependently increased phase II of the migrating motor complex. The contraction frequency increased slightly at the highest dose, but neither motility index nor contraction amplitude changed. It is concluded that neurokinin A and substance P stimulate small intestinal motility in man, and it can be speculated that they play a role in the control of human small intestinal motility.

Adult↗