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PubMed1999

Relationship of Helicobacter pylori infection with gastrointestinal motility.

The interest of gastroenterologists in the relationship between Helicobacter pylori and gastrointestinal motility emerges from the observation that Helicobacter pylori may be involved in the pathogenesis of functional dyspepsia and that a relatively large percentage of patients with dyspepsia may show impaired gastrointestinal motility. A number of studies have been published on the interaction between Helicobacter pylori infection and gastrointestinal motility with controversial results, and, therefore, there are no definite conclusions, as yet, as to whether Helicobacter pylori is able, at all, or in which degree, to influence the motility of the upper gastrointestinal tract. Motility of the upper gastrointestinal tract has been studied in Helicobacter pylori positive and negative individuals by means of manometry, scintigraphy, radio-opaque markers or by other, recently developed, procedures such as breath tests, ultrasonography, and barostat. The vast majority of studies do not support the hypothesis that Helicobacter pylori may influence gastrointestinal motility. Nearly all these studies are, however, affected by methodological problems related to the small numbers of patients, different methodological approaches, and to the well-known difficulties in studying both gastrointestinal motility and functional dyspepsia.

Dyspepsia↗

PubMed1996

Gastrointestinal motility in neonatal and pediatric practice.

Caring for children with gastrointestinal motility disorders requires an understanding of age-related changes in gastrointestinal function and in the clinical expression of disease. Successful evaluation of the child with a gastrointestinal motility disorder necessitates an approach that takes into account not only the child's symptoms, but also the stage of development. This article reviews the ontogeny of gastrointestinal motility; the techniques available for the study of gastrointestinal motility in children; and the presentation, pathophysiology, and treatment of pediatric functional bowel diseases. Differences in children compared to adults in performing and analyzing motility testing and in evaluating motility disorders are emphasized. A more complete understanding of pediatric motility disorders may provide important insights in approaching functional bowel diseases in adults.

Adult↗

PubMed1975

Influence of sulpiride on gastrointestinal motility: experimental radiological study in the dog.

A radiological study has been carried out in the dog to control the influence of N-ethyl-2(2-methoxy-5-sulfamido-benzamidomethyl)-pyrrolidine (sulpiride) on the motility of the gastrointestinal tract. The drug was administered orally and parenterally at different doses for each pharmaceutical form and for such route of doses for each pharmaceutical form and for each route of administration. In doses which were considered optimal, the results have demonstrated that sulpiride exerts hypertonic and hyperphasic effects on the smooth musculature of the gastrointestinal tract. Consequently, there is a reduction of the transit time and of the emptying of the opaque meal in the various sectors of the gastrointestinal tract, which is in the order of about 50% with respect to normal. Using doses which are inferior to those considered optimal, no significant results were obtained, while following higher doses the action of sulpiride is manifested by an inhibitory effect on gastrointestinal motility.

Administration, Oral↗

PubMed1992

[An experimental study of gastrointestinal motility during chronic large bowel obstruction].

Gastrointestinal motility and plasma PYY levels were investigated under chronic progressive large bowel obstruction in dogs. The obstruction device was applied around the descending colon at a laparotomy and gastrointestinal motility was recorded with strain gauge force transducers in the conscious state. Complete obstruction occurred at 26 days (21-33 days). The duration of postprandial interruption of motor complex (DIMC) in the antrum and duodenum were prolonged progressively, at partial obstruction (17.7 +/- 2.7 hr; p less than 0.05) and complete obstruction (23.0 +/- 4.0 hr; p less than 0.01) vs in control (13.7 +/- 1.9 hr), while DIMC in the small bowel showed no significant changes. Progressive obstruction caused hypermotility in the proximal colon to the obstruction and hypomotility in the distal colon. These dysmotility were improved after resection of the obstructed segment and anastomosis. Plasma PYY levels in the fasting state showed no significant increase at complete obstruction (42.6 +/- 14.5 pmol/l) vs in control (32.9 +/- 10.2 pmol/l).

Animals↗

PubMed2002

Screening and identification of proteins mediating senna induced gastrointestinal motility enhancement in mouse colon.

AIM: To isolate the proteins involved in pharmacologic action of senna extract (SE) from mouse gastrointestinal tract and to explore the molecular mechanism of gastrointestinal motility change induced by SE. METHODS: SE was administrated to mice by different routes. Gastrointestinal motility of mice was observed using cathartic, gastrointestinal propellant movement experiments and X-ray analysis. Mouse model for gastrointestinal motility enhancement was established through continuous gastric administration of SE at progressively increased dose. At 3 h and week 3, 4, 6 and 10, morphological changes of gastrointestinal tissues were found under light microscope. Ultrastructural changes of intestinal and colonic tissues at week 6 were observed under transmission electron microscope. The colonic proteomic changes in model mice were examined by two-dimension polyacrylamide gel electrophoresis with immobilized pH gradient isoelectric focusing to screen the differentially expressed proteins, and their molecular masses and isoelectric points were determined. Two N-terminal sequences of the samples were also determined by mass spectrometry. RESULTS: SE (0.3g) caused diarrhea after gastric administration in 1-6h and enhanced gastrointestinal propellant (65.1+/-7.5%; 45.8+/-14.6%, P<0.01) in mice, but intramuscular and hypodermic injection had no cathartic effect. X-ray analysis of gastrointestinal motility demonstrated that gastric administration of SE enhanced gastric evacuation and gastrointestinal transferring function. At 3 h and week 3 and 4 after gastric administration of SE, light microscopic examination revealed no apparent change in gastrointestinal mucosal tissues, but transmission electron microscopic examination revealed inflammatory changes in whole layer of intestinal and colonic wall. Twenty differential proteins were detected in the colonic tissues of the model mice by two-dimensional electrophoresis, and the N-terminal amino acid sequences of two proteins were determined. CONCLUSION: SE causes diarrhea and enhances gastrointestinal motility through digestive tract administration. Long-term gastric administration of SE induces inflammatory changes and cell damage in the whole gastrointestinal tract. The differential proteins screened from the colonic tissues of the model mice might mediate the enhancing effect of SE on gastrointestinal motility.

Animals↗

PubMed1995

Effect of endotoxin on canine gastrointestinal motility and transit.

Ileus is common during sepsis; however, the etiology of this gastrointestinal dysmotility is unclear. The aim of our study was to determine the effects of a single, sublethal dose of endotoxin on canine gastrointestinal motility, gastric emptying, gastric acid secretion, and colonic transit. Six dogs underwent placement of manometric catheters in the stomach and small bowel and insertion of a gastric and a cecal cannula. After the animals recovered, fasting and fed gastrointestinal motility was recorded, and gastric emptying and colonic transit were studied with nonabsorbable liquid and solid markers, respectively. Following completion of baseline studies, each dog was given a single dose of Escherichia coli lipopolysaccharide (200 micrograms/kg intravenously) and the studies were repeated on Postendotoxin Days 1-3. The single bolus of endotoxin abolished the migrating motor complexes, decreased the fasting motility index, decreased hydrogen ion output, slowed liquid gastric emptying, and prolonged colonic transit for 2 days. Gastrointestinal motility and transit returned to baseline on Postendotoxin Day 3. In conclusion, a single, sublethal dose of endotoxin temporarily disrupts fasting and postprandial canine gastrointestinal motility and transit.

Animals↗

PubMed1993

Gastrointestinal motility disorders during pregnancy.

PURPOSE: To review the pathophysiology of gastrointestinal motility disorders during pregnancy, their clinical manifestations, and their management. DATA SOURCES: Studies published from 1963 to 1992 identified by computerized literature searches of Index Medicus and MEDLINE; hand searches; contact with pharmaceutical representatives for information on drug therapy during pregnancy; and selected texts on drugs and obstetrics. STUDY SELECTION: Selected studies were those involving controlled design of physiology related to pregnancy or to hormonal effects on the gastrointestinal tract or both, and clinical studies or previous reviews that contributed to the understanding of the gastrointestinal effects of pregnancy. DATA EXTRACTION: Data concerning the epidemiology, causes, clinical manifestations, and complications of altered gastrointestinal motility during pregnancy as well as the strength of association between gastrointestinal disorders of pregnancy and hormonal changes were evaluated and used to develop a practical approach to evaluate and manage these patients. RESULTS OF DATA SYNTHESIS: Effects on the gastrointestinal tract during pregnancy are caused primarily by hormonal changes and not the physical effects of the gravid uterus. Motility changes occur throughout the gastrointestinal tract, including a reduction in lower esophageal sphincter pressure and its physiologic function with resulting gastroesophageal reflux and the risk for aspiration; alterations in gastric motor function associated with nausea and vomiting; and a decrease in the rate of small-bowel and colonic transit manifested primarily as abdominal bloating and constipation. These effects are mediated by progesterone, with estrogen probably acting as a primer. CONCLUSIONS: Given the large number of pregnancies each year complicated by gastrointestinal motility disorders, many physicians (including internists and gastroenterologists) must manage these problems. Knowledge of the underlying physiologic alterations in gastrointestinal motility during pregnancy and of safe treatment options is essential to the care of the pregnant patient.

Animals↗

PubMed1983

Disorders of gastrointestinal motility associated with diabetes mellitus.

Gastrointestinal symptoms such as vomiting, constipation, diarrhea, and fecal incontinence occur frequently in patients with diabetes mellitus. In a survey of 136 diabetic outpatients, 76% had one or more gastrointestinal symptoms, the commonest symptom being constipation (found in 60%). In many cases these symptoms are thought to be due to abnormal gastrointestinal motility that, in turn, may be a manifestation of diabetic autonomic neuropathy involving the gastrointestinal tract. The pathophysiology of these gastrointestinal symptoms, clarified in recent studies, and the clinical features and treatment of these problems in diabetic patients are reviewed.

Autonomic Nervous System Diseases↗

PubMed1986

Gastrointestinal motility disorders.

A classification of gastrointestinal motility disorders is offered based upon the type of disorder in transit (delay or acceleration), and the region of the gastrointestinal tract affected. Specific abnormalities of myoelectrical patterns are identified when possible and related to disturbances in transit in the stomach and small bowel.

Animals↗

PubMed1987

Stimulation of gastrointestinal motility by loperamide in dogs.

The effects of loperamide on gastrointestinal motility were investigated in conscious fasted dogs chronically fitted with strain-gauge transducers on the antrum, the jejunum, and the colon. Oral administration of loperamide (0.1 mg/kg) induced, after a delay of 20-30 min, a long-lasting (8-12 hr) stimulation of gastrointestinal motility associated with a disorganization of the cyclic activity at the three levels investigated. These effects were reproduced by a subcutaneous administration at the same dose and were antagonized by previous intravenous administration of naloxone or a quaternary opiate antagonist. Intracolonic administration (0.1 mg/kg) stimulated, after a delay of 20-30 min, colonic motility only. Intracerebroventricular loperamide (1 microgram/kg) induced a long-lasting (15-20 hr) inhibition of the gastric motility and a short (2-hr) disorganization of the jejunal motor profile. These data show that oral loperamide stimulates gastrointestinal motility in dogs and involves peripheral opiate receptors.

Administration, Oral↗

PubMed1989

Postprandial gallbladder filling: relation to gastrointestinal motility.

A technique of combined hepatobiliary scintigraphy and gastrointestinal motility recordings was used to study the relationship between gallbladder dynamics and gastrointestinal motility recordings in the postprandial state in eight healthy male volunteers. In all, a fed-like motility pattern was observed after ingestion of a standard meal, and all activity from the HIDA-scintigraphy was diverted to the duodenum. Gallbladder radioactivity on the scintigram was not seen until 145-249 (median, 180) min after ingestion, except for two cases in which an early and transient activity was seen. Together with increasing gallbladder radioactivity characteristic changes in duodenal motility occurred. In five subjects a decrease in motility index was encountered with a motility curve resembling phase I of the interdigestive migrating motor complex. In one subject it was associated with the appearance of a phase-III complex, and in two subjects it occurred without any changes in motility index.

Adult↗

PubMed1989

Effects of pharmacological agents on gastrointestinal motility.

The control mechanisms of gastrointestinal motility are complex. Extrinsic neurohormonal effects modulate an intrinsic system, often called the "gut brain," composed of nervous and neuropeptide components. To exert pharmacologic influence on GI motility, use is made of agents that mimic the external control system. Agents that stimulate opioid receptors, block adrenoceptors, block or facilitate acetylcholine action, or antagonize the action of prostaglandins are used to effect changes in GI motility. The major indications for pharmacologic intervention are to increase motility in constipation, to reduce it in most cases of diarrhea, and to restore propulsive coordination in postoperative ileus. In cases of clinical colic the primary requirement is control of pain. Agents used for this purpose may adversely affect motility, and choice requires knowledge of their actions in this respect. In addition, drugs used for other purposes, anthelmintics for instance, may also influence gut motility. A synopsis of the actions of the agents commonly employed in GI motility control and some associated drugs are displayed in Table 3. Recent advances in the understanding of drug action on the gut should help in the selection of drugs for clinical use.

Animals↗

PubMed1986

Relationship between impaired gastric emptying and abnormal gastrointestinal motility.

The mechanism of gastric stasis in disorders of gastrointestinal motility is largely unexplored. The region or regions of abnormal motility in 13 patients with a gastrointestinal motility disorder were characterized manometrically. Antral hypomotility was established in 6 patients and intestinal dysmotility in 7 others. One patient had both antral hypomotility and intestinal dysmotility. Gastric emptying of solids and liquids was quantitated scintigraphically; emptying data for solids were represented by a two-phase model (lag and emptying) and for liquids by a power exponential model. Antral hypomotility was associated with gastric stasis manifested by both a prolongation of the solid lag time [from 35 +/- 6 min for controls to 87 +/- 23 min (mean +/- SE), p less than 0.05] and slower emptying rates of solids (from a slope index of 29.9 +/- 2 for controls to 17.8 +/- 5, p less than 0.05) and liquids (from a kappa index of 3.6 +/- 0.6 for controls to 1.5 +/- 0.5, p less than 0.05). Intestinal dysmotility did not alter the solid lag time; however, it did decrease the slope of solid emptying from the stomach (from a slope index of 29.9 +/- 2 for controls to 13.5 +/- 3, p less than 0.05) and also prolonged emptying of liquids (from a kappa index of 3.6 +/- 0.3 for controls to 1.9 +/- 0.6, p less than 0.05). These data are consistent with the hypothesis that the gastric stasis in gut dysmotilities occurs because of impaired antral peristalsis due to antral hypomotility or increased resistance to flow into the small bowel due to intestinal dysmotility.

Adult↗

PubMed1992

[Gastrointestinal motility and autonomic nerve dysfunction].

Gastrointestinal motility is greatly influenced by both the autonomic nervous system (ANS) and the enteric nervous system (ENS). Dysfunction of ANS and/or ENS produces various kinds of dysmotility from the esophagus to the colon. Generalized autonomic dysfunction, often seen in diabetics, causes abnormal peristaltic waves in the esophagus, abnormal electrical activity of the stomach, delayed gastric emptying and delayed intestinal transit. Localized disorders of the enteric nervous system is seen in patients with achalasia and Hirschsprung's diseases. Functional disorders, without evidence of organic disorders, like non-cardiac chest pain, non-ulcer dyspepsia, irritable bowel syndrome, can be partly caused by abnormal function of autonomic nervous system.

Autonomic Nervous System↗

PubMed1975

[The effects of flavoxate hydrochloride on the gastrointestinal motility (author's transl)].

The experiments were performed to study the effects of Flavoxate hydrochloride on the gastrointestinal motility and its underlying mechanism. Gastrointestinal motility was inhibited at first and then accelerated markedly after the intravenous injection of Flavoxate hydrochloride (10 mg/kg) in the experiments of anesthetized dogs. For analyzing the underlying mechanism of this response the following experiments were executed. 1) The pendular movements of isolated ileum of rabbits were accelerated with administration of low concentration of Flavoxate hydrochloride less than 10(5) g/ml, while these were reduced with administration of high concentration more than 10(4) g/ml. Because the tetrodotoxin (2.5 times 10(7) g/ml) has no essential effect on these responses, it could be postulated that Flavoxate hydrochloride has direct effect on intestinal smooth muscle itself. 2) Flavoxate hydrochloride (10 mg/kg) induced the differentiated regional response of the sympathetic outflow, that is, the parallel decrease of cutaneous and cardiac sympathetic activities, and the converse increase of splanchnic activity. Therefore, Flavoxate hydrochloride is thought to have an effect on the integrating mechanism of the sympathetic nervous system. This view was also supported by the experiments with neuromuscular preparation of lobster (Panulirus japonicus). It is concluded from these results, that the change of gastrointestinal motility induced by intravenous injection of Flavoxate hydrochloride (10 mg/kg) is influenced both by its effect on the gastrointestinal smooth muscle itself and by its effect via the autonomic nervous system.

Animals↗

PubMed1989

An erythromycin derivative, EM-523, induces motilin-like gastrointestinal motility in dogs.

The effect of an erythromycin derivative, EM-523, on gastrointestinal motility was investigated in conscious dogs and compared with that of motilin cisapride, trimebutine and metoclopramide. In the fasting state, EM-523 given i.v. or i.d. at 3 micrograms/kg or more induced contractions in the stomach that migrated along the small intestine. The pattern of the contractions was very similar to that induced by motilin. In the digestive state, EM-523 increased the amplitude of gastric contractions. Cisapride and metoclopramide increased gastrointestinal motility both in the fasting and digestive states; however, their contractile pattern was different from that of EM-523. Trimebutine did not induce gastric motility in the fasting state but rather decreased gastric motility in the digestive state. The contractions induced by EM-523 and motilin were inhibited by atropine but were not affected by naloxone, suggesting that the cholinergic pathway is important in the exertion of their action. These results indicate that EM-523 mimics motilin in stimulating gastrointestinal motility and that this agent may be useful treat gastrointestinal disorders such as gastric stasis, gastroesophageal reflux, and postoperative ileus, and so forth.

Animals↗

PubMed2002

[Genetic basis of autonomic gastrointestinal motility and pathophysiological models].

The origin of rhythmicity in gastrointestinal motility was long thought to involve the activity of interstitial cells of Cajal (ICC) that locate in close association with enteric neurons and smooth muscle cells. We have demonstrated that significant decrease in the number of cells immunopositive to c-Kit, a type of tyrosine kinase receptor, in the gastrointestinal tract of mice mutated at the W/c-kit locus and BALB/c mice administered with neutralizing c-Kit antibody leads to the impaired autonomic motility of the gastrointestinal tract. It is also demonstrated that ICC express c-kit which plays important roles in development and maintenance of the ICC network in the gastrointestinal tract. ICC, derived from mesenchymal cells, are classified into smooth muscle type and fibroblast type by their morphology and tissue location. The ligand for c-Kit, Sl factor (SLF), has shown to be expressed in enteric neurons and gastrointestinal smooth muscle cells. Studies with mutant mice and transgenic mice have suggested that functional c-Kit/SLF is required for the differentiation and proliferation of ICC as pacemakers and mediators of neural regulation in gastrointestinal motility. Here we review the genetic basis of autonomic gastrointestinal motility and the pathophysiological models.

Animals↗

PubMed2002

Beer congener stimulates gastrointestinal motility via the muscarinic acetylcholine receptors.

BACKGROUND: Ethanol and alcoholic beverages are known to affect upper gastrointestinal motility in humans. Beer has been reported to accelerate gastric emptying compared with other beverages that contain the same ethanol concentrations. In this study, we investigated the mechanism that underlies the effects of beer congener on gastrointestinal motility. METHODS: Gastric emptying activity was measured by means of movement of a semisolid test meal (0.05% phenol red/1.5% methylcellulose) in mice. To elucidate the mechanism for the effect of beer congener on gastrointestinal motility, we conducted receptor binding assays and contraction study by using longitudinal muscle from guinea pig ileum. RESULTS: Beer congener (1 g/kg orally) enhanced gastric emptying of a semisolid meal in mice. The receptor binding assay revealed that beer congener bound to dopamine D2 receptor and 5-hydroxytryptamine (5-HT)3 receptor. These IC50 values were more than 5 mg/ml. However, beer congener bound to 5-HT2 receptor, 5-HT4 receptor, and muscarinic M3 receptor with IC50 values of 2, 0.9, and 2 mg/ml, respectively. Beer congener (0.05-2 mg/ml) induced the contraction of longitudinal muscle from guinea pig ileum in a dose-dependent manner. This effect was not affected by either tetrodotoxin (10(-6)M) or ketanserin (10(-7)-10(-5)M), an antagonist for the 5-HT2 receptor. On the other hand, 4-DAMP (10(-8)-10(-5)M), an antagonist for the muscarinic M3 receptor, inhibited the contraction of the longitudinal muscle induced by beer congener (2 mg/ml) dose dependently. CONCLUSIONS: Beer congener stimulates gastrointestinal motility via the muscarinic M3 receptor.

Animals↗