Small Intestinal Motor Activity Research Articles

Effect of mebeverine hydrochloride on jejunal motility and epithelial transport in the anesthetized ferret

Previous in vitro and in vivo studies demonstrate that mebeverine, administered to isolated smooth muscle preparations or given intravenously, (i.v.), acts as an antispasmodic agent and may be useful in treating intestinal hypermotility. Whether mebeverine affects intestinal mucosal transport is, however, unknown. The aim of the present study was to characterize the effect of mebeverine on both small intestinal motor activity and electrogenic epithelial transport in the urethane anesthetized ferret. The effects of mebeverine were compared following i.v. and intrajejunal (i.j.) administration. Following both routes of drug administration mebeverine dose dependently inhibited jejunal motility, with the i.j. route being more potent. However, when administered i.v. but not i.j., the doses of mebeverine that inhibited jejunal motility also significantly reduced heart rate and arterial blood pressure. Mebeverine (0.1–10 mg/kg) administered i.v. had no significant effect on epithelial transport as measured by a change in transmural potential difference. However, when dosed i.j., mebeverine (0.1–10 mg/kg) induced a decrease in potential difference towards lower lumen negativity, which was suggestive of a decrease in fluid secretion or enhancement of absorption. In conclusion, the results confirm in vivo the antispasmodic effect of mebeverine and suggested that mebeverine can influence epithelial transport, probably in the direction of enhanced intestinal absorption.

Human small intestinal motor activity and postprandial glycemia after dietary fiber intake

Human small intestinal motor activity and postprandial glycemia after dietary fiber intake

The migrating myoelectric complex of the small intestine.

Gastric and small intestinal myoelectric and motor activity is divided into two main patterns, fed and fasted. During fasting, the predominant pattern of activity is the migrating myoelectric complex (MMC), a cyclically occurring pattern of electric and mechanical activity that is initiated in the stomach and duodenum almost simultaneously and, from there, propagates the length of the small intestine. Cyclic motor activity also occurs in the lower esophageal sphincter, the gallbladder, and the sphincter of Oddi with a duration that is related to the MMC in the small intestine. Of the possible mechanisms for initiation of the MMC in the small intestine (extrinsic neural control, intrinsic neural control, and hormonal control), intrinsic neural control via a series of coupled is the most likely. The keep this sentence in! hormone motilin also plays a role in the initiation of MMCs. After a meal, in man the MMC is disrupted and replaced by irregular contractions. The physiologic role of the MMC is to clear the stomach and small intestine of residual food, secretions, and desquamated cells and propel them to the colon. Disruption of the MMC cycle is associated with bacterial overgrowth in some patients, an observation that supports the proposed cleansing function of the MMC cycle.

Trichinella spiralis infection alters small bowel motor activity in the fed state

The effect of Trichinella spiralis infection on small intestinal transit and motor activity in the fed state during the intestinal phase of infection was studied. Contractions were recorded by strain gauge transducers, and mean transit time was measured by marker dilution technique. The mean amplitude and area of individual phasic contractions decreased, but no change occurred in their mean duration during trichinosis. The total amplitude and area of phasic contractions also decreased; this was caused by a decrease in the frequency of contractions as well as a decrease in the mean parameters. The reduction in the total duration was entirely caused by the decrease in frequency. The reduction in the total parameters of all contractions was the result of a reduction in the same parameters for both propagating and nonpropagating contractions. However, the decrease in the parameters of propagating contractions was much greater. Also, there was a decrease in the distance of propagation of phasic contractions. The transit time as a result of phasic contractions increased during T. spiralis infection. Additionally, T. spiralis infection induced giant migrating contractions in the fed state that were never observed during control. Chyme was propelled very rapidly and effectively by giant migrating contractions. The findings of the present study suggest that during diarrhea induced by T. spiralis infection, the phasic contractions may act to decrease transit and, hence, allow more contact time for absorption of water and nutrients. However, this response may be counter-balanced by giant migrating contractions that rapidly propel chyme into the colon and compound the diarrhea associated with T. spiralis infection.

Effects of CCK receptor blockade on intestinal motor activity in conscious dogs

This study employed a cholecystokinin (CCK) antagonist to evaluate whether endogenous CCK regulates fasted and fed motor patterns of the small intestine. Experiments were performed in six conscious dogs, each in duplicate. Motor activity was recorded by six strain-gauge transducers implanted along the small intestine. The effects of the CCK analogue caerulein and the CCK antagonist loxiglumide were studied in fasted and fed states. Computer analysis determined contractile frequency and area under contractions. Caerulein given as an intravenous bolus 30 min after phase III dose dependently caused a burst of phasic contractions preceded by a retrograde giant contraction. Continuous intravenous infusion of 10 mg.kg-1.h-1 loxiglumide completely abolished the effects of 10 ng/kg caerulein, which increases plasma CCK immunoreactivity to postprandial levels. Loxiglumide, at 10 mg.kg-1.h-1, markedly reduced the increase in phasic contractions due to a supraphysiological dose of 50 ng/kg caerulein to 14 +/- 6(SD)% of the control without loxiglumide (P less than 0.01). The motor activity stimulated by the cholinesterase inhibitor neostigmine (10 micrograms/kg) was not altered by loxiglumide. Loxiglumide given in the fasted state decreased contractile frequency from 9.5 +/- 0.7 to 8.1 +/- 0.6/min and reduced the area under contractions during phase II to 81 +/- 5% of the control without loxiglumide (P less than 0.05). Loxiglumide also decreased contractile frequency during the fed state from 9.7 +/- 0.6 to 8.3 +/- 0.5/min and reduced the area under contractions to 78 +/- 6% of the control without loxiglumide (P less than 0.05). Thus loxiglumide acts as a specific antagonist of the actions of CCK on small intestinal motor activity in the dog. Loxiglumide, at a dose that abolishes actions of endogenous CCK, significantly decreased fasting motor activity during phase II. Loxiglumide also significantly reduced motor responses to feeding but did not prevent interruption of migrating motor complex cycle by a meal. CCK plays a physiological role in regulation of fasting and fed motor activity of small intestine, although other factors in addition to CCK mediate meal-induced motor activity.

Effect of T. spiralis infection on intestinal motor activity in the fasted state

We sought to determine the effects of Trichinella spiralis infection on small intestinal motor activity in the fasted state in dogs and relate it to clinical symptoms during the intestinal phase of trichinosis. Motor activity was recorded by strain gauge force transducers. Infection with T. spiralis resulted in a significant increase in the incidence and proximal origination of giant migrating contractions (GMCs) during the first 5 days postinfection. This was also the time when the dogs had diarrhea. The dogs were often restless and showed signs of discomfort during proximally originating GMCs. The incidence of retrograde giant contractions (RGCs) increased significantly on the 2nd and 3rd day postinfection. RGCs were followed by vomiting 71% of the time during infection. The migrating motor complex cycle length increased significantly, and this was due to intestinal "amyogenesia" and "dysmyogenesia". During these phenomena, electrical control activity was almost completely obliterated in the proximal half of the small intestine (amyogenesia) and became irregular and unstable in the distal half (dysmyogenesia). Intestinal amyogenesia and dysmyogenesia lasted up to 4 h and were terminated by a GMC. We conclude that diarrhea induced by T. spiralis infection is closely associated with an increase in the incidence and proximal origin of GMCs. These GMCs may also be the motor correlates of abdominal cramping and pain during the intestinal phase of trichinosis.

Relation between small intestinal motor activity and transit in secretory diarrhea

Our objective in this study was to correlate small intestinal motor activity with transit time in the fed state under normal conditions and in the secretory state induced by cholera toxin. In the control state, transit time was strongly and inversely correlated with the mean distance of propagation and to a lesser degree with frequency and total duration of all contractions. By contrast, transit time was not correlated with total amplitude and area of all contractions. When contractions were separated into propagating and nonpropagating contractions, there was a highly significant inverse correlation between transit time and all parameters of propagating contractions but no relation with any parameter of nonpropagating contractions. Similar results were obtained during the secretory state induced by cholera toxin. The control data were used to develop a mathematical model to predict transit time from contractile parameters and was validated using the data obtained in the secretory state. Our findings demonstrate that transit through the small intestine in the normal and secretory states is strongly related to the parameters of propagating contractions but not to parameters of nonpropagating contractions.

Medullary sites mediating some abdominal vagal reflexes in the ferret using [ 14C]2-deoxyglucose

The central projections of some abdominal visceral afferents passing through the vagal communicating branch were studied in anesthetized ferrets using [ 14C]2-deoxyglucose autoradiography. The reflex effects of electrical stimulation of the vagal communicating branch were studied while measurements of jejunal motor activity and transmural potential difference, a marker of electrogenic epithelial transport were made concurrently. The aim of this study was to examine brainstem projections of some afferent fibers in the communicating branch of the thoracic vagus nerve that are necessary for the reflex regulation of small intestinal motor activity and epithelial transport. In urethane-anesthetized ferrets, electrical stimulation of the cur central end of the vagal communicating branch increased jejunal motor activity and electrogenic epithelial transport. In addition, glucose utilization in the left medial sub-nucleus of the nucleus tractus solitarius and the dorsal motor nucleus of the vagus was significantly increased as compared with sham-operated non-stimulated control animals. Identical areas on the contralateral side of the brain showed no change in glucose utilization as compared with sham-operated non-stimulated controls. This functional brain-mapping study strongly suggests that the left medial sub-nucleus tractus solitarius and the dorsal motor nucleus of the vagus, in the ferret, are involved in processing alimentary affrent activity from both the small intestinal musculature and epithelium as well as the reflex changes in efferent vagal nerve activity to the same regions of the alimentary tract.

Effect of cholera toxin on small intestinal motor activity in the fed state

We sought to determine the effect of cholera toxin on small intestinal transit and motor activity in the fed state. Mean transit time increased after cholera toxin, but there was no change in mean amplitude, duration, and area of contractions. In contrast, there was a reduction in the total amplitude, duration, and area of contractions, and this was due to a decrease in frequency of contractions. The reduction in the total parameters of all contractions could be accounted for by a reduction in the same parameters for propagating contractions. The parameters of nonpropagating contraction were not different after cholera toxin. Also, there was a decrease in the distance of propagation of contractions. Our findings demonstrate that during the secretory state due to cholera toxin the small intestinal motor activity works in a compensatory mode to decrease transit and allow more time for absorption.

Effect of somatostatin on gallbladder volume and small intestinal motor activity in humans

The effects of different doses of somatostatin (36, 180, 360 pmol/kg/h) on the motor patterns of the duodenum and on gallbladder volume in the postprandial period were evaluated. Gallbladder volume and small intestinal motor activity were monitored simultaneously in 9 normal subjects. Gallbladder volume was measured every 5 min throughout the study by real-time ultrasonography while intestinal motility was recorded manometrically by means of a lowcompliance pneumohydraulic system. On day 1, the response of the gallbladder to a 972-kcal test meal was evaluated ultrasonographically to assure a normal response. On day 2, at least 2 consecutive phase III complexes of the interdigestive motor cycle were recorded. Gallbladder volume varied cyclically during the interdigestive motor cycle, with the minimum value late in phase II and the maximum early in phase I (p < 0.01); the test meal was then administered. Following the induction of a typical pattern of postprandial motility, somatostatin infusion was started and continued for 150 min. Somatostatin, at the 180- and 360-pmol/kg/h doses, interrupted the fed pattern and induced consecutive bursts of propagated clustered activity. The characteristics of these somatostatin-induced motor patterns were similar to the spontaneous phase III of the interdigestive motor cycle. An initial reduction in gallbladder volume followed the ingestion of the meal; during somatostatin infusion, gallbladder volume increased to values greater than fasting values and varied cyclically with minimum values before the second episode of propagated clustered activity. These results show that somatostatin interrupts the fed pattern and elicits consecutive clusters of propagated motor activity in the duodenum that are coordinated with cyclic fluctuations in gallbladder volume.

Effects of Cholera Toxin on Small Intestinal Motor Activity in the Fasted State

We sought to determine the effect of cholera toxin on small intestinal motor activity in the fasted state and relate it to secretion in conscious dogs. Motor activity was recorded by strain gauge force transducers and secretion was measured by diverting it to the outside through a two‐way cannula. Inoculation of the study segment with cholera toxin resulted in a 10‐fold increase in fluid output by 120 minutes postinjection. At the same time that fluid output increased Significantly changes in fasting motor activity occurred. The cycle length of the migrating motor complex was significantly reduced, the percentage of phase II activity was significantly increased, and migrating clustered contractions were inhibited. Perfusion of the study segment by a nonabsorbable electrolyte solution at a rate similar to the rate of secretion induced by cholera toxin did not change the cycle length of migrating motor complexes, but the percentage of phase II activity was significantly increased as with cholera toxin, and migrating clustered contractions were inhibited. The reduction in the cycle length of migrating motor complexes seems to be a direct effect of cholera toxin on the gut wall while the increase in percentage of phase II activity and inhibition of migrating clustered contractions appear to be indirect effects due to fluid accumulation.

Thyrotropin‐Releasing Hormone Potently Modulates Peristaltic Motor Activity of the Guinea Pig Small Intestine

Thyrotropin‐releasing hormone (TRH) is present in enteric neurons of the guinea pig intestine, which indicates it may have a role in the control of gut motility. Isolated segments of the guinea pig duodenum‐jejunum and ileum were used to examine the effect of TRH on intestinal peristalsis. The peristaltic waves in the proximal small intestine were triggered at a higher intraluminal pressure and exhibited a higher frequency and a lower amplitude than those in the ileum. TRH (0.3–300 nM) induced a concentration‐related increase in the pressure threshold at which peristaltic waves were elicited and a moderate decrease in the amplitude of the peristaltic waves in both regions. However, while the frequency of the peristaltic waves was increased by the peptide in the ileum, it was diminished by TRH (0.3 and 3 nM) in the duodenum‐jejunum. Since the contractile effect of carbachol on the circular muscle of the duodenum‐jejunum remained unaffected by TRH, it appears that the peptide does not act on the muscle directly but influences peristalsis by acting on enteric neurons. The data further suggest that TRH released from enteric neurons may play a physiologic role in the regulation of propulsive motor activity of the gut.

Effect of pacing on small intestinal motor activity and hormonal response in dogs

In seven beagle dogs with a Thiry-Vella loop, the effect of pacing on small intestinal motor activity was examined by means of extraluminal strain gauge force transducers. Recordings were obtained from the loop and from the remaining small intestine. Our study showed that pacing of the loop results in a significant reduction of the motility of the loop in the overnight fasted state (up to 39%), during loop feeding (up to 55%), and oral feeding (up to 39%); a similar reduction of the motility of the remaining small intestine (up to 43%); and a significant postprandial increase of insulin (9.0 microU/ml) and decrease of glucagon (94 pg/ml). The motility reduction of the loop and of the remaining small intestine as well as the anabolically improved pancreatic endocrine function (shown by an increase of the insulin-glucagon ratio) suggests that this form of pacing could be of benefit for motility disorders with decreased transit time.

Effects of fractionated doses of ionizing radiation on small intestinal motor activity

The small intestinal motor effects of fractionated doses of ionizing radiation were studied in 6 conscious dogs. Eight strain-gauge transducers were implanted on the small intestine and a single gauge on the ascending colon, of each dog. After control recordings, an abdominal dose of 250 cGy was administered three times a week on alternate days for 3 successive weeks (total dose, 2250 cGy). Recordings were then made for 4 wk of follow-up. Giant migrating contractions occurred 11 times in 520 h of control recordings in the fasted and fed state, with a mean distance of origin of 55 ± 16 cm from the ileocolonic junction. Abdominal field irradiation significantly increased the incidence and distance of origin of these giant contractions to 438 in 745 recording hours and 158 ± 7 cm from the ileocolonic junction, respectively. The incidence of giant migrating contractions peaked after the second dose of radiation. The amplitude ratio of radiation-induced giant migrating contractions to phase III contractions, and their duration and velocity of migration, were similar to the control state. The dogs developed diarrhea and vomiting as early as the first fraction of radiation. Irradiation also increased the incidence of retrograde giant contractions from 8 in 520 h of control recording to 42 in 745 h of recording during the radiation schedule. The radiation-induced retrograde giant contractions peaked in incidence on the day of the first fraction of radiation and were more likely to be associated with a vomiting episode than those occurring in the control period. Migrating motor complex cycling persisted during radiation and its cycle length was not different from the control or postradiation values. Our findings suggest that some of the side effects of radiation such as diarrhea, abdominal cramping, and vomiting may be related to the dramatically increased incidence of giant migrating contractions and retrograde giant contractions.

Peptide YY (PYY) stimulates intrinsic enteric motor neurones in the rat small intestine.

The effects of peptide YY (PYY) on motor activity of the rat small intestine, were studied using isolated organ bath preparations arranged for recording muscle activity in the longitudinal axis. PYY induced TTX sensitive concentration-dependent contractions and/or relaxations of the longitudinal muscle in different regions of the small intestine. In the duodenum PYY evoked only "cholinergic" contractions (3 x 10(-8)-3 x 10(-7) M). In the jejunum, PYY-evoked concentrations were non-cholinergic, and contractions were never seen in the ileum. In the jejunum and ileum, PYY-evoked relaxations (3 x 10(-8)-3 x 10(-7) M) were unaffected by adrenoceptor or cholinergic receptor blockade, thus indicating that these relaxations were mediated by non-adrenergic, non-cholinergic (NANC) inhibitory nerves. Another action of PYY was to cause inhibition of field stimulation-evoked cholinergic concentrations. This inhibitory action was primarily due to antagonism of post-junctional, cholinergic receptor mediated events. In addition, PYY inhibited histamine evoked contractions of the longitudinal muscle. All regions of the small intestine could be desensitized to PYY. Such PYY-densensitization did not affect the ability of the longitudinal muscle to relax in response to applied ATP or papaverine. These results suggest PYY has potent concentration-dependent stimulatory actions at intrinsic inhibitory and excitatory motor nerves. In addition, PYY interferes with contractions but not relaxations of the longitudinal muscle.

25 PERSISTENT FEEDING PROBLEMS AFTER CORRECTION OF INTESTINAL MALROTATION – MANOMETRIC ASSESSMENT

Top of pageAbstract The introduction of feeds after correction of a midgut malrotation is usually uneventful but may be difficult in a small number of cases. The nature or the intrauterine migration defect is unknown. We assessed small intestinal motor activity manometrically in five children (mean age 13.6 mths) with persistent feeding problems after correction at a mean time of 13.0 mths after surgery. Two groups were noted. Four children with persistent vomiting did not tolerate oral feeds. All of these had a second surgical procedure attempting to relieve an obstruction (2 a pyloromyotomy, 1 an ileocaecal resection, 1 an ileostomy) but continued to have symptoms. Tnree had abnormal small intestinal motility, one no activity, one slow Phase III pressure wave frequency with short Phase III duration, and one non-propagated Phase III complexes with a low motility index (MI). One child (number 5) had severe diarrhoea after feeds due to a short bowel syndrome following an ileal resection after a volvulus. This child had a low motility index in Phase III. Tnese data show that a pattern of motor activity similar to that seen in intestinal neuropathic disorders is present in these patients. We speculate that the malrotation is secondary to a neuropathic disorder present during early foetal development in some patients.

Ontogeny of fasting small intestinal motor activity in the human infant.

A clearly defined progression of fasting small intestinal motor development is seen in the human infant from disorganised low amplitude motor activity before 31 weeks gestation through an intermediate phase of increasing motor organisation and amplitude to the development of a normal cyclical pattern of motor activity with clearly defined phase I, II, and III activity between 37 weeks gestation and term. With increasing maturity smooth muscle contractility [gastric antral pressure (5-30 mmHg), average duodenal pressure (2-12 mmHg)], propagation and slow wave frequency (10.5-12.5 cpm) all increased in a significant fashion (p less than 0.01). The stage of development of fasting motor activity in the small intestine of the preterm infant can now be readily predicted from the gestational age of the infant.

Measurement of small-intestinal motor activity in the preterm infant

The development of motor activity within the small intestine of preterm human infants is very poorly understood. Using a miniaturized multilumen continuous perfusion manometric technique the motor activity of the small intestine was followed longitudinally in a group of preterm infants. The system performed well at very low perfusion rates and clearly showed increases in both the magnitude and organization of motor activity with increasing gestational age.

Small Intestinal Motor Activity — Its Role in Gut Homeostasis and Disease

The study of small intestinal motor activity has certainly emerged from relative obscurity to a position where it may indeed become an important clinical tool. Modern technology has led to a considerable increase in our understanding of the physiology of motor function and has brought us to a stage where small intestinal motility is amenable to study in man. It is clear that coordinated motor function of the small intestine is central to integrated digestive function. Normal patterns, and in particular normal variants, are still being defined, and both the investigator and the clinician need to be particularly aware of interspecies, intersubject and interregional variations. While in some instances, abnormal motility is clearly related to an underlying disorder of intestinal neuromuscular function, in others, and in particular in functional gastrointestinal disorders, the overall experience of intestinal motility recordings in man is still too limited to allow us to declare with confidence whether reported abnormalities are, indeed, truly aberrant patterns or whether they are causally related to a given patient's symptoms.

The development of small intestinal motor activity in the premature infant : J.B. Watt, W.M. Bisset, R.P.A. Rivers and P.J. Milla, St Mary's Hospital Medical School, London W2 and The Institute of Child Health, London WC1, U.K.

The development of small intestinal motor activity in the premature infant : J.B. Watt, W.M. Bisset, R.P.A. Rivers and P.J. Milla, St Mary's Hospital Medical School, London W2 and The Institute of Child Health, London WC1, U.K.