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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↗

PubMed2006

Pediatric gastrointestinal motility--future directions and challenges.

The study of gastrointestinal motility has evolved to a sophisticated diagnostic technique that is widely used clinically to further guide management of children with complex gastrointestinal problems. Thorough comprehension requires a multidisciplinary approach with the integration of molecular and cell biology, organ physiology, and clinical observations. During the past decade there has been a dramatic increase in our knowledge of the enteric neuromuscular system. Continued exploration of targeted gene mutations in animal models has the potential of enhancing our understanding of congenital disorders of gastrointestinal motility. Experiments studying polymorphisms in serotonin transporter gene (SERT) and different therapeutic responses to serotonergic agents in adults with irritable bowel syndrome need to be carried out in children with functional bowel disorders. Additional considerations that need to be addressed if advances are to continue include increasing the number of specialists interest in motility disorders and identifying funding sources to support the establishment of research consortiums among pediatric centers.

Child↗

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↗

PubMed1994

Cisapride. An updated review of its pharmacology and therapeutic efficacy as a prokinetic agent in gastrointestinal motility disorders.

Cisapride is an orally administered prokinetic agent which facilitates or restores motility throughout the length of the gastrointestinal tract. It is a substituted piperidinyl benzamide, chemically related to metoclopramide, but unlike metoclopramide, cisapride is largely devoid of central depressant or antidopaminergic effects. In placebo-controlled trials, cisapride improved healing rates and symptoms in both adults and children with reflux oesophagitis. Maintenance therapy with cisapride at half the healing dose is effective in reducing the incidence of relapse. Symptoms are also alleviated in patients with functional dyspepsia, and gastric emptying and symptoms are improved in most patients with gastroparesis, an effect which is sustained during long term administration. However, the efficacy of cisapride in end-stage gastroparesis remains less clear. Cisapride increases stool frequency in patients with chronic constipation, and limited data suggest that the drug may also be beneficial in treating chronic intestinal pseudo-obstruction and irritable bowel syndrome. Cisapride demonstrated efficacy comparable with or superior to that of metoclopramide, and was at least as effective as cimetidine and ranitidine in patients with reflux disease. In patients with functional dyspepsia, cisapride has shown at least equal efficacy to domperidone, metoclopramide and ranitidine, and superior efficacy to cimetidine in the small comparative trials conducted to date. Adverse effects in patients receiving cisapride are generally transient and mild, with abdominal cramping, borborygmi, diarrhoea or loose stools most frequently reported. Central nervous system adverse effects are rare. Thus, with its favourable tolerability profile and demonstrated efficacy in a variety of gastrointestinal motility disorders, the position of cisapride as a valuable agent in the management of patients with gastrointestinal motility disorders is strengthening. However, larger well-controlled comparative trials of the drug with other agents are necessary before the relative position of cisapride in therapy can be categorically defined.

Animals↗

PubMed2006

Equine gastrointestinal motility--ileus and pharmacological modification.

Colic is a common problem encountered in equine practice. Alteration of gastrointestinal motility is often the underlying cause for abdominal pain. Gastrointestinal motility can be measured as myoelectric activity, mechanical activity, and transit of intraluminal contents. Regulation of motility is based on a complex interaction between central innervation, autonomic innervation, and the enteric nervous system. Various humoral and neurochemical substances are required to interact flawlessly to allow propulsive motility. Ileus is defined as the absence of propulsive aboral movement of gastrointestinal contents, irrespective of its pathophysiology. Potential etiologies for ileus are described in this review. The prokinetic drugs available for clinical use are discussed. Choosing the appropriate prokinetic drug requires knowledge about the complex nature of gastrointestinal motility and its abnormalities.

Abdominal Pain↗

PubMed1979

[Effect of reduced gastrointestinal motility on the regulation of gastrointestinal flora and the pathogenesis of coli enterotoxinemia in market swine].

Opium tincture and Spasmentral were applied to piglets early after weaning and reduced their gastro-intestinal motility, which, however, caused only very minor changes in quantitative germ flora composition in those first days. Short-time suppression of gastro-intestinal motility obviously does not result in detrimental consequences to the organism as a whole, since there seem to be several factors which are involved in the control and regulation of the intestinal germ flora. Impairment of gastro-intestinal motility appeared to be of no importance to the pathogenesis of coli-enterotoxaemia, as it was not followed by higher incidence of the disease.

Animals↗

PubMed2002

[Gastrointestinal motility and vegetative balance: correlations in peptic ulcer].

To evaluate changes in gastrointestinal motility and their correlations with vegetative dysfunction in duodenal ulcer, computed electrogastroenterography was made in 22 healthy subjects, 23 patients with uncomplicated duodenal ulcer and 45 patients with duodenal ulcer complicated by fat hepatosis, chronic cholecystitis and/or biliary dyskinesia, chronic pancreatitis, reflux esophagitis. The study was also made of the vegetative tonicity, vegetative reactivity, circadian urine excretion of vanilylmandelic acid. It was discovered that uncomplicated duodenal ulcer is characterized by intensive gastrointestinal motility correlating with parasympathicotonia and vegetative hyperreactivity. In patients with complicated duodenal ulcer gastric and intestinal motor activity is weaker than in patients with uncomplicated ulcer. They have parasympathicotonia and low vegetative reactivity but gastrointestinal motility does not depend much on functional state of the autonomic nervous system.

Adolescent↗

PubMed1979

A study of the effect of vinca alkaloid 'vinblastine' on gastrointestinal motility in rats.

Vinblastine an alkaloid of the periwinkleplant (Vinca), produced marked alterations in the motility of gastrointestinal tract in rats. The alkaloid reduced the rate of gastric emptying and slowed the transit of test substance through the small intestine. The effect of the drug on gastric emptying appeared to be dose-dependent. The latency of drug action on gut motility was found to be 5--10 min, when injected through the jugular vein.

Animals↗

PubMed2002

Anticholinergic suppression of fetal rabbit upper gastrointestinal motility.

OBJECTIVE: At birth the newborn digestive tract must assume the responsibility of assimilating nutrients for survival. Immature gastrointestinal motility in the neonate may result in impaired feeding and nutrition. Newborn gastrointestinal motility development requires the expression and functional maturation of gastrointestinal receptors. To explore the timing of fetal responses to gastrointestinal cholinergic motility agents, we assessed the effect of the anticholinergic agent atropine in the late-gestation rabbit fetus. METHODS: Seven pregnant New Zealand White rabbits were studied at day 30 of their normal 31-day gestation. In each litter, two fetuses were selected as study (n = 14) and two as control (n = 14). Under ultrasound guidance, a spinal needle was percutaneously inserted through the maternal uterus into the fetal stomach and 0.5 ml of gastric content was aspirated. Fluorescein, labelled with colored microspheres, and either atropine (0.04 microg/g fetal body weight) or normal saline were injected in a total volume of 0.5 ml. Two hours after injection, fetuses were delivered, the small intestine harvested, and the total small intestinal length and the distance the gastrointestinal fluorescein travelled were measured by ultraviolet light optical density. The fluorescein travelled distance and the per cent motility, defined as the length of fluorescein travelled divided by the total length of the small intestine, were calculated. RESULTS: All fetuses survived the intragastric injection. Mean fetal body weight at delivery was 44.2 +/- 6.7 and 46.8 +/- 7.2 g in atropine and control fetuses, respectively. The fluorescein travelled distance (15.4 +/- 4.2 vs. 19.0 +/- 4.3 cm;. p < 0.01) and per cent motility (51.0 +/- 8.9 vs. 63.8 +/- 11.7%; p < 0.01) of atropine-treated fetuses were significantly lower than those of control fetuses. CONCLUSION: Fetal upper gastrointestinal motility is suppressed in response to intragastric atropine. These results indicate that fetal gastrointestinal cholinergic receptors are expressed and functional in the term (0.97 gestation) rabbit fetus. In utero administration of cholinergic agonists/antagonists may potentially modulate fetal gastrointestinal motility and absorption of amniotic fluid water and solutes.

Animals↗

PubMed1985

Action of enkephalinergic neurons on the gastrointestinal motility.

The actions of the enkephalinergic neurons in the myenteric plexus on the gastrointestinal motility were studied using the opiate antagonist naloxone in the guinea pig in vitro and in vivo. Naloxone increased or decreased spontaneous contractions of the isolated small intestine. Both responses were abolished by atropine. Naloxone potentiated or inhibited the twitch response to transmural stimulation at a frequency of 0.1 Hz and the contractile response of the ileum to the mesenteric nerve stimulation. Naloxone reversed an inhibition of the twitch response occurred after repetitive transmural stimulation (10 Hz) for 5 minutes in the isolated ileal segment. The peristaltic reflex response in the isolated jejunum induced by its distention was reduced by repeated distention. This reduction was reversed by naloxone. Naloxone also potentiated the contractile response of the stomach to efferent vagal stimulation in vivo. It is concluded from the present results that enkephalinergic neurons in the myenteric plexus may regulate the gastrointestinal motility by inhibiting release of acetylcholine from myenteric cholinergic neurons, and that naloxone has both opiate antagonistic and partial agonistic effects on the gastrointestinal motility of the guinea pig.

Animals↗

PubMed2003

Neurohumoral control of gastrointestinal motility.

Neurohumoral substances and their receptors play a major part in the complex regulation of gastrointestinal motility and have therefore been the predominant targets for drug development. The numerous receptors involved in motility are located mainly on smooth muscle cells and neuronal structures in the extrinsic and intrinsic parts of the enteric nervous system. Within this system, receptor agonists and antagonists interacts directly to modify excitatory or inhibitory signals. In view of this complexity it is not surprising that our knowledge about the mechanisms of actions of the various neurohormones and drugs affecting gut motility has been rather fragmented and incomplete. However, recently substantial progress has been achieved, and drug therapy for gut dysmotility is emerging, based primarily on neurohumoral receptors. This paper presents a selective review of the neurohumoral regulatory mechanisms of gastrointestinal motility. In this context, the physiology and pharmacology of the smooth muscle cells, gastrointestinal motility and dysmotility, the enteric nervous system, gastrointestinal reflexes, and serotonin is presented. Further investigation and understanding of the transmitters and receptors involved in especially the reflex activation of peristalsis is crucial for the development of novel therapies for motility disorders.

Animals↗

PubMed1994

Pharmacokinetic drug interactions with gastrointestinal motility modifying agents.

Drugs may affect gastrointestinal motility and, therefore, absorption of other concomitantly administered drugs. Gastrointestinal prokinetic agents increase the rate of gastric emptying and also upper intestinal motility. These effects would be expected to increase the initial rate of absorption of orally administered drugs, but reduce total bioavailability of the agents. Metoclopramide has been shown to increase the rate of absorption of several classes of drug, reflected by reduced time taken to achieve maximal plasma concentration (tmax) and increased maximal plasma concentration (Cmax). However, the effect of these agents on the area under the plasma concentration-time curve from zero to infinity (AUC0-infinity), when measured, is not consistent. Cisapride and domperidone appear to have similar effects, but there are relatively less data available regarding these products. Opioids may delay gastric emptying considerably, an effect which will often have significant clinical and therapeutic implications. Most of the data confirming this observation concern oral analgesics, but the effect should be considered when prescribing any oral medication. Drugs with anticholinergic or sympathomimetic activity are likely to have a similar effect and this is confirmed, in the main, by the limited data available. Although many effects reported in the literature are of limited clinical importance, they may be significant when prescribing a drug with a narrow therapeutic index, especially if it is absorbed poorly.

Absorption↗

PubMed1993

Assessment of upper gastrointestinal motility in the cancer-associated dyspepsia syndrome.

Cancer patients experience many gastrointestinal symptoms which may lead to weight loss. Assessment of gastrointestinal motility may contribute to our understanding of these symptoms and suggest rational therapeutic approaches to the anorexia-cachexia syndrome. We have evaluated a simple, inexpensive, well-tolerated test of upper gastrointestinal motility in patients with advanced cancer. One-centimetre portions of radiopaque nasogastric tubing were ingested with food. Six hours later, a flat-plate abdominal x-ray was obtained to determine the marker placement. Patients were evaluated for gastrointestinal symptoms. Those with more symptoms, particularly early satiety, had a greater incidence of reduced upper gastrointestinal motility.

Adult↗

PubMed1998

Effect of capsaicin-containing red pepper sauce suspension on upper gastrointestinal motility in healthy volunteers.

Afferent nerves play a major role in the regulation of gastrointestinal motility. The questions remains if specific food ingredients can selectively activate such fibers. The aim of the study was to investigate the effect of intraesophageal application of a capsaicin-containing red pepper sauce (Tabasco) suspension on upper gastrointestinal motility in a controlled trial. After a baseline recording [esophageal motility, balloon distension, electrogastrogram (EGG)], red pepper or saline solution was infused intraesophageally in seven healthy volunteers. At 30 min gastric emptying and orocecal transit time were determined using a [13C]acetate and H2-lactulose breath test. Infusion of red pepper sauce suspension significantly increased the amplitudes (65.8 +/- 3 to 78.5 +/- 4.7 mm Hg, P < 0.05) and propagation velocity (2.9 +/- 0.3 to 4.25 +/- 0.3 sec, P < 0.05) of esophageal pressure waves and LES pressure (17.8 +/- 1.4 to 23.7 +/- 2.6 mm Hg, P < 0.05). It significantly decreased perception and discomfort threshold of intraesophageal balloon distension, reduced the percentage of normal electrical activity in the EGG, and delayed gastric emptying (saline: T(1/2) 42.9 +/- 12.0 min vs red pepper: T(1/2) 66.8 +/- 19.0 min, P < 0.05). Despite the prolongation of gastric emptying, orocecal transit time was not altered, indicating an actual increase of intestinal transit. Esophageal application of capsaicin-containing red pepper sauce suspension had profound changes on upper gastrointestinal motility, which could improve clearance and protection of the esophagus and could lead to retention of the irritant in the stomach and faster transit through the small bowel.

Adult↗

PubMed1996

Recovery of fasted and fed gastrointestinal motility after open versus laparoscopic cholecystectomy in dogs.

OBJECTIVE: The authors investigate the recovery of gastrointestinal motility in the fed and fasted state after laparoscopic and open cholecystectomy. SUMMARY BACKGROUND DATA: Clinical recovery after laparoscopic cholecystectomy is known to be more rapid than after conventional open cholecystectomy. However, the actual effect of a laparoscopic approach on gastrointestinal motility, particularly fed-state motility, is not well investigated. METHODS: Laparoscopic (LAP, n=6) or open (OPEN, n=6) cholecystectomy was performed in 12 dogs. Bipolar recording electrodes were placed on the antrum, small intestine, and the transverse and descending colon, and fasting myoelectric data were recorded after operation. Solid meal gastric emptying studies were performed before surgery and on postoperative days 1 and 2. Transit time studies were performed using 10 radiopaque markers. RESULTS: Gastric emptying was significantly delayed in the OPEN group at 120 minutes on postoperative day 1 compared with pre-operative emptying (p<0.05), but was not delayed on postoperative day 2. Gastric emptying was not delayed in the LAP group after operation. Transit time was the same between groups. Gastric dysrhythmias were more frequent on postoperative day 3 (p<0.05) in the OPEN group. There were no significant differences in the presence, cycle length, or propagation velocity of the migrating motor complex on any postoperative day. Discrete or continuous electrical response activity in the colon was observed by postoperative day 1 in both groups. CONCLUSIONS: Fed-state motility is the only parameter for which laparoscopic cholecystectomy showed an improvement in postoperative recovery. Recovery of fasted gastrointestinal motility in dogs is equally rapid after either operation.

Animals↗