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At least 217 records · Page 12Linked to original sources
PubMed1993

A double-blind fluoroscopic study of cisapride on gastrointestinal motility in patients with functional dyspepsia.

Twenty patients with functional dyspepsia were referred for radiologic examination and, upon confirmation of a hypomotile stomach, were given either 10 mg cisapride or placebo in a double-blind manner (10 patients per group). The movement of a 250-ml barium meal was assessed by means of television fluoroscopy performed at regular time intervals. Cisapride significantly improved antral contractility and enhanced gastric emptying compared with placebo. Deep peristaltic waves occurred over the entire small bowel, and motility and small-bowel transit time of the barium meal were significantly increased in the cisapride group compared with the placebo group. The study demonstrates that when a carefully defined protocol is observed, fluoroscopy following barium ingestion offers considerable potential in the assessment of gastrointestinal motility.

Barium Sulfate↗
PubMed1984

Effects of ranitidine and oxmetidine on gastrointestinal motility in conscious dog.

Two histamine H2-receptor antagonists ranitidine and oxmetidine were tested for their effects on gastrointestinal motility in conscious fasted dogs chronically fitted with intraparietal electrodes on the antrum, duodenum and jejunum. Intravenous administration of ranitidine (3 mg/kg) stimulated gastrointestinal spiking activity through a cholinergic mechanism and increased the duration of the cycles of migrating myoelectric complexes. Oxmetidine at the same dose did not modify the gastrointestinal motor profile. These results showed clearcut differences in nonspecific effects of two H2-antagonists equipotent on gastric acid secretion.

Animals↗
PubMed1990

Gastrointestinal motility enhancing effect of ginger and its active constituents.

The effect of ginger root (Zingiberis Rhizoma) on gastrointestinal motility was examined based on its ability to enhance charcoal meal transport in mice. Oral administrations of the acetone extract of ginger (which contains volatile oils and bitter substances) at 75 mg/kg, [6]-shogaol at 2.5 mg/kg, or a [6]-, [8]- or [10]-gingerol at 5 mg/kg enhanced the transport of a charcoal meal. The effects of these substances were similar to or slightly weaker than those of metoclopramide and donperidone.

Animals↗
PubMed1980

Actions of motilin on gastrointestinal motility and plasma immunoreactive motilin concentration in interdigestive and postprandial states.

Among biological actions of motilin on gastrointestinal motility, its action to induce phase III, activity front, of interdigestive myoelectric complex (IMC) appears to be of physiological significance. Synthetic motilin in a dose as little as 0.06 microgram/kg-h was shown to induce phase III in dog. A cyclic increase in fasting plasma immunoreactive motilin concentration (PIMC) occurred in phase III in dog and in a later part of phase II in man, suggesting strongly that there is an intimate relationship between cyclic increase in fasting PIMC and IMC. The observation also suggested that gastric acid secretion increases in phase II and phase III of IMC. The cyclic increase in the acid secretion may be related to a coincidental cyclic increase in PIMC. Ingestion of a meat meal results in a significant decrease in PIMC and abolishes the cyclic increase in PIMC, while IMC changes to digestive pattern after a meal. The significant decrease in PIMC is not attributed to the 3 known gut hormones including gastrin, octapeptide of CCK and secretin.

Animals↗
PubMed1991

[Effect of motilin agonist, EM-523 on gastrointestinal motility].

In this study, we investigated the effect of EM-523, one of the erythromycin derivatives, on gastrointestinal motility in conscious dogs, in which force transducers were chronically implanted in the gastrointestinal tract. As a result, intravenous administration of EM-523 (1-10 micrograms/kg) induced phase III-like contractions in the stomach, and the EM-523-induced contractions migrated along the entire small intestine. EM-523 also stimulated the lower esophageal sphincter and the gallbladder motility, quite similar to exogenous motilin. Furthermore, we have investigated the effects of EM-523 both in postoperative ileus dogs and truncally vagotomized dogs. The dogs 1 to 4-day after the operation showed continuous and irregular contractions in the entire gastrointestinal tract, instead of typical interdigestive contractions. In these conditions, EM-523 induced strong phasic contractions in the stomach and duodenum, although these contractions did not always migrate along the small intestine. In the vagotomized dogs, spontaneous phase III contractions tended to be weaker than those in the normal dogs. EM523 induced phase III-like contractions in vagotomized dogs as in the normal dogs, and the contractile activities were improved. These results indicated that EM-523 may be useful as a gastroprokinetic drug for postoperative ileus and the patients with vagotomy.

Animals↗
PubMedDate not supplied

Pharmacological regulation of postprandial gastrointestinal motility by glucagon in conscious dogs.

The physiological or pharmacological role of glucagon in the postprandial regulation of gastrointestinal motility has not yet been clarified. To clarify it, the following experiments were performed on conscious dogs. Antral, duodenal, jejunal and ileal contractile activities were monitored by chronically implanted strain gauge force transducers without restraint. The serum gastrin concentration in response to ingestion was measured by radioimmunoassay. 1) When glucagon (5 approximately 50 microg/kg, drip infusion for 5 minutes) was administered before ingestion of meal or 2 hours after ingestion, it inhibited postprandial motility dose-dependently in the antrum, while enhancing it in the duodenum, jejunum and ileum. 2) At the same time, glucagon inhibited the meal induced elevation of the serum gastrin concentration. 3) On the other hand, glucagon did not inhibit the contractions induced by pentagastrin (4 microg/kg,s.c.) or those induced by acetylcholine chloride (0.5 mg/kg, drip infusion for 10 minutes) in any region. 4) These glucagon-induced inhibitory effects in postprandial antral motility were not affected by phentolamine (0.5 mg/kg, i.v.) or nitro-L-arginine-methyl ester (L-NAME) (3 mg/kg/hr, drip infusion for 30 minutes). These results suggest that: 1) Glucagon inhibits the postprandial elevation of the serum gastrin concentration and thus inhibits postprandial antral motility. 2) On the other hand, in the intestine, glucagon-induced inhibitory responses might be reversed by glucagon-induced excitatory responses through preganglionic cholinergic motor neurons. 3) The mechanism of inhibition of gastrin release was not definite in my experiments, but one of the candidates may be activation of somatostatin release from the D cells by glucagon.

Animals↗
PubMed2005

Effects of isoflurane on gastrointestinal motility after brief exposure in rats.

In pre-clinical studies, investigation of oral formulations often necessitates the use of general anesthesia to facilitate deposition of material directly into the stomach. Since the effectiveness of intestinal drug absorption is dependent on gastric emptying (GE) and intestinal motility, drugs that influence either will also influence drug absorption. This study investigated gastrointestinal motility in rats after brief exposure to Isoflurane (ISO) general anesthesia for orogastric gavage. The use of metochlopramide was also evaluated. Twenty-five fasted rats were induced with brief ISO anesthesia (<6 min). Rats were gavaged a gelatin capsule (8mm (L) x 2.0mm (o.d.)) containing 9 mg of activated charcoal powder (gastrointestinal marker) and rapidly recovered. Gavage was performed using a 15 cm feeding device with a soft hollow tip to hold the capsule. Study included three groups (60 and 120 min recovery, metochlopramide pre-treatment with 60 min recovery) and control. Animals were sacrificed for exposure and examination of the gastrointestinal tract following the allocated recovery period. Gastrointestinal transit of charcoal was reduced approximately 50% 120 min after brief ISO anesthesia. Metochlopramide pre-treatment did not increase gastrointestinal propulsion despite increased GE. These data warrant consideration in intestinal drug absorption studies where ISO is the anesthetic of choice.

Animals↗
PubMed2006

Long-term signal detection, segmentation and summarization using wavelets and fractal dimension: a bioacoustics application in gastrointestinal-motility monitoring.

The current paper describes a wavelet-based method for long-term processing and analysis of gastrointestinal sounds (GIS). Windowing techniques are used to select sequential blocks of the prolonged multi-channel recordings and proceed to various wavelet-domain processing stages. De-noising, significant-activity detection, automated segmentation and extraction of summary curves are applied in an integrated mode, allowing for enhanced content manipulation and analysis. The proposed analysis scheme combines flexible long-term graphical representation tools, while maintaining the ability of quick browsing via visualization and auralization of the detected short-term events. This work is part of a project aiming to implement non-invasive diagnosis over gastrointestinal-motility (GIM) physiology. However, the proposed techniques might be applied to any study of long-term bioacoustics time series.

Algorithms↗
PubMed1993

Gastrointestinal motility in patients with non-ulcer dyspepsia: a role for Helicobacter pylori infection?

Motor disorders of the upper gastrointestinal tract are a frequent finding in patients with non-ulcer dyspepsia (NUD). In this study we attempted to assess whether Helicobacter pylori infection contributes to gastrointestinal motor disorders in NUD. Interdigestive and post-prandial gastrointestinal motility was studied in 46 consecutive patients with NUD and in eight healthy control subjects. Abdominal complaints were assessed by means of a symptom score. Chronic gastritis and H. pylori infection were assessed and graded by histology. Accordingly, patients with NUD were divided into two sub-groups: 18 patients with H. pylori infection and chronic active gastritis and 28 patients without H. pylori infection. The length of the interdigestive motor cycle was not different in patients with NUD (139 +/- 6 min, mean +/- SEM), compared with controls (128 +/- 5.5 min). There was also no difference in the duration of individual phases I, II, and III, either between NUD and controls or between H. pylori-positive and -negative patients. The motility index (MI) of antral phase II also was not changed in NUD patients. Postprandial antral motility was decreased in patients with NUD (MI 6.96 +/- 0.4 vs. 9.7 +/- 0.3 controls; p < 0.025), with no difference between H. pylori-positive and -negative subgroups. It therefore appears unlikely that H. pylori infection plays a primary role in the pathophysiology of antroduodenal motor disorders in NUD.

Adult↗
PubMedDate not supplied

Involvement of cholinergic motor neurons in pharmacological regulation of gastrointestinal motility by glucagon in conscious dogs.

UNLABELLED: To clarify the exact mechanisms of the pharmacological effects of glucagon on gastrointestinal motility, the following experiments were performed on the conscious and anesthetized dogs. 1) During phase I of interdigestive migrating contractions (IMC), glucagon (5 approximately 50 microg/kg, drip infusion for 5 minutes) induced phasic contractions in the duodenum, jejunum and ileum, but not in the antrum. These excitatory responses were also observed in the truncal vagotomized dogs. These contractions were abolished by atropine or hexamethonium in the conscious dogs, and also by tetrodotoxin in the anesthetized dogs. 2) Glucagon inhibited cisapride-induced contractions only in the antrum in the conscious dogs. After pre treatment with hexamethonium, glucagon inhibited these contractions in the duodenum, jejunum and ileum as well as in the antrum. After pre treatment with tetrodotoxin in the anesthetized dogs, glucagon did not affect acetylcholine induced contractions in any region. 3) Glucagon inhibited spontaneous phase III contractions and erythromycin induced phase III like contractions in the antrum, but did not inhibit either contractions in the other regions in the conscious dogs. These paradoxical effects of glucagon between the antrum and intestine were similar to those involved in the blockade of 5-hydroxytryptamine 3 receptors. After pre-treatment with hexamethonium, glucagon inhibited these contractions in the duodenum, jejunum and ileum as well as in the antrum. IN CONCLUSION: 1) Glucagon latently inhibits cholinergic motor activities in the antrum and intestine not directly, by binding to either receptor on the smooth muscle cells, but through postganglionic cholinergic neurons and possibly through 5-hydroxytryptamine neurons. 2) On the other hand, in the intestine the reverse effects through preganglionic cholinergic neurons involving nicotinic and muscarinic receptors are more potent. 3) As a result, glucagon inhibits antral contractions and does not affect intestinal contractions in a conscious state.

Animals↗
PubMed1995

Gastrointestinal motility in the neonate.

Although patterns of gastrointestinal movements have been recognized for nearly a century, only in the past 10 years have we had the diagnostic tools to characterize both normal and abnormal motility in the neonate. Parallel with these advances, over the past 25 years, we have seen an explosion in our understanding of the ENS and its independent regulation of gut motility. It is expected that, as we come to a better understanding of the microregulation of intestinal motor activity, we can develop more effective means to treat many of these heretofore refractory disorders of gastrointestinal motility.

Animals↗
PubMed2005

Mechanisms for modulation of mouse gastrointestinal motility by proteinase-activated receptor (PAR)-1 and -2 in vitro.

Proteinase-activated receptor (PAR)-1 or -2 modulates gastrointestinal transit in vivo. To clarify the underlying mechanisms, we characterized contraction/relaxation caused by TFLLR-NH2 and SLIGRL-NH2, PAR-1- and -2-activating peptides, respectively, in gastric and small intestinal (duodenal, jejunal and ileal) smooth muscle isolated from wild-type and PAR-2-knockout mice. Either SLIGRL-NH2 or TFLLR-NH2 caused both relaxation and contraction in the gastrointestinal preparations from wild-type animals. Apamin, a K+ channel inhibitor, tended to enhance the peptide-evoked contraction in some of the gastrointestinal preparations, whereas it inhibited relaxation responses to either peptide completely in the stomach, but only partially in the small intestine. Indomethacin reduced the contraction caused by SLIGRL-NH2 or TFLLR-NH2 in both gastric and ileal preparations, but unaffected apamin-insensitive relaxant effect of either peptide in ileal preparations. Repeated treatment with capsaicin suppressed the contractile effect of either peptide in the stomach, but not clearly in the ileum, whereas it enhanced the apamin-insensitive relaxant effect in ileal preparations. In any gastrointestinal preparations from PAR-2-knockout mice, SLIGRL-NH2 produced no responses. Thus, the inhibitory component in tension modulation by PAR-1 and -2 involves both apamin-sensitive and -insensitive mechanisms in the small intestine, but is predominantly attributable to the former mechanism in the stomach. The excitatory component in the PAR-1 and -2 modulation may be mediated, in part, by activation of capsaicin-sensitive sensory nerves and/or endogenous prostaglandin formation. Our study thus clarifies the multiple mechanisms for gastrointestinal motility modulation by PAR-1 and -2, and also provides ultimate evidence for involvement of PAR-2.

Animals↗
PubMed1988

Effect of cisapride on the cholinergic control mechanisms of gastrointestinal motility in dogs.

The action of cisapride on physiological and disturbed gastrointestinal motor function was investigated in conscious and anesthetized dogs and the mechanism of action involved. Regardless of the presence or absence of vagal innervation, administration of cisapride (0.2 mg approximately 1.0 mg/kg body weight, i.v.) during the quiescent period of interdigestive migrating contractions (IMC), induced non-migrating IMC-like motility in the entire gastrointestinal tract from gastric body to distal colon. Administration of cisapride in the digestive state resulted in the excitatory response of increased amplitude of digestive peristalsis and strong IMC-like motility was not observed. All of these excitatory responses in gastrointestinal motility disappeared by the administration of atropine (0.5 mg approximately 0.1 mg/kg body weight, i.v.). Furthermore, the excitatory response in gastrointestinal motility induced by cisapride in anesthetized dogs disappeared by the administration of TTX (10 micrograms/kg of body weight, i.v.). These results suggest that the excitatory action of cisapride on the gastrointestinal motility is based on its mechanism in which cisapride acts on the cholinergic neurones in the gastrointestinal wall to stimulate ACh release, resulting in the increase in gastrointestinal motility. Cisapride caused powerful IMC-like motility in the ileum of animal with pseudo-obstruction-like motor disturbance which had been seen after preparation of Thiry loop (ileum). This motility migrated from the proximal ileum to the Thiry loop and then to the distal ileum. Trimebutine maleate also demonstrated this effect, but metoclopramide and domperidone were ineffective. Administration of cisapride at the doses (0.2 mg approximately 1.0 mg/kg body weight, i.v.) causing stimulated motor response in the gastrointestinal tract did not induce significant secretion of gastric acid, pancreatic juice and bile.

Animals↗
PubMed2006

Magnet Tracking: a new tool for in vivo studies of the rat gastrointestinal motility.

Digestive motility was studied in the rat using a miniaturized version of the Magnet Tracking system which monitored the progression of a small magnetic pill through the entire digestive tract. The dynamics of movement was followed and three-dimensional (3-D) images of digestive tract were generated. After a retention period in the stomach and rapid passage through duodenum, the magnet progressed along the small intestine with gradually decreasing speed and longer stationary periods. It remained in the caecum for variable intervals. In the colon, periods of progress alternated with long quiescent periods. Gastric activity oscillated at 5-6 min(-1). In the small intestine, two frequency domains coexisted, showing independent modulations and proximo-distal gradients (40 to >32 and 28 to >20 min(-1)). Caecal oscillations were of 1.5 min(-1). The data allowed the magnet location and calculation of gastric and small intestinal transit times (58 +/- 36 and 83 +/- 14 min respectively), both significantly prolonged by oleate administration (243 +/- 130 and 170 +/- 45 min respectively). Magnet Tracking is a non-invasive tool to study the in vivo spatial and temporal organization of gastrointestinal motility in the rat.

Animals↗