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At least 145 records · Page 8Linked to original sources
PubMed2001

Effect of Helicobacter pylori infection on gastrointestinal motility, pancreatic secretion and hormone release in asymptomatic humans.

BACKGROUND: Helicobacter pylori infection is associated with complex alterations of the gastric physiology in patients with ulcer disease or functional dyspepsia. We aimed at evaluating whether H. pylori infection is accompanied by changes in interdigestive and postprandial gastrointestinal motility, exocrine pancreatic secretion or hormone release in asymptomatic subjects. METHODS: Nineteen healthy men (age range 26-35 years) were studied after 12 h fasting. Motor activity was recorded for a complete motor migrating complex cycle and two postprandial hours. Pancreatic enzyme secretion was evaluated using a standard duodenal perfusion technique. Plasma concentrations of gastrin, PP and motilin were determined at 15-min intervals. H. pylori infection was proved by serology and 13C-urea breath test. RESULTS: Eight subjects (42%) were H. pylori positive. Interdigestive and postprandial gastrointestinal motility were similar in H. pylori positive and negative subjects. Interdigestive pancreatic secretion was increased in H. pylori positive subjects (P < 0.05). Postprandial pancreatic secretion tended also to be higher in H. pylori positive subjects. H. pylori infection was associated with an increased postprandial release of gastrin (P < 0.05) as well as with a slight increase of interdigestive gastrin release. The release of PP and motilin, as well as the interdigestive coordination between gastrointestinal motility, pancreatic secretion and hormone release, was not altered by H. pylori infection. CONCLUSIONS: H. pylori infection in asymptomatic subjects is associated with changes not only in gastric physiology but also in pancreatic function. This first reported link between H. pylori and the pancreas could have pathophysiological implications in pancreatic diseases and therefore deserves further study.

Adult↗
PubMed1990

Gastrointestinal motility disorders in diabetes mellitus.

Gastrointestinal motor abnormalities are common in patients with diabetes mellitus and may result in significant morbidity. Patients may present with a wide range of symptoms, including manifestations of organ involvement or poor glucose control. Derangements of motility may result in complicated and difficult management problems. This paper reviews the clinical features, pathophysiology, and treatment of diabetic gastrointestinal motility disorders.

Diabetes Complications↗
PubMed2004

[Effect of dachengqi granule on human gastrointestinal motility].

OBJECTIVE: To study the therapeutic effect and mechanism of Dachengqi granule (DCQG) on some digestive motility disturbed diseases. METHODS: Gastroduodenojejunal manometry, electrogastrography (EGG), RIA of motilin and orocecal transit time test were applied to directly observe the effect of DCQG on human gastrointestinal motility. RESULTS: DCQG could significantly improve the postoperational EGG disorder, elevate the amplitude and time of migrating motor complex (MMC) phase III, prevent gastrointestinal reversed peristalsis, increase the blood level of motilin, decrease the orocecal transit time, and promote the recovery of gastrointestinal motility. CONCLUSION: DCQG is an effective digestive kinetic agent, which could be medicated conveniently in treating digestive motility disturbed diseases.

Adult↗
PubMed2006

[Researches on automatic analyzing system of the whole gastrointestinal motility recordings].

Many diseases of gastrointestinal tract have close relation to the changes in gastrointestinal (GI) motility. Making use of the technique of MEMS, we developed a micro-interposed system to monitor the motility and pH value of the whole GI tract under normal physical state. This paper focuses on an automatic analysis of the acquired signal to draw conclusions for aiding diagnosis of diseases. The techniques of smoothing signal, removing singular value, feature extraction and selection as well as classification of normal and abnormal samples are discussed in details. These techniques provide a comprehensive method for analyzing long-term motility recordings which will complete the function of the in vivo monitoring system and serve for medical applications.

Gastrointestinal Diseases↗
PubMed1985

The influence of a chronic subclinical infection of Trichostrongylus colubriformis on gastrointestinal motility and digesta flow in sheep.

The influence of a chronic subclinical infection of Trichostrongylus colubriformis, 2500 larvae/day for 12 weeks, on gastrointestinal motility and digesta flow was studied in 12 sheep supplied ad libitum with food and water. Motility was recorded by X-radiography and electromyography from chronically implanted electrodes; abomasal volume and outflow were estimated by dilution of CrEDTA; small intestinal transit time was estimated by passage of Phenol Red. The findings were compared with measurements made prior to infection at restricted food intake and reported separately. The first effects of infection were seen after 3-4 weeks. No animal developed diarrhoea, but food intake was progressively reduced. Small intestinal transit time, abomasal volume and half-time of marker dilution increased while abomasal outflow decreased during infection. These changes occurred both in absolute terms and when compared with values predicted from the observed level of food intake. As the animals became resistant to the parasites abomasal volume and digesta flow returned towards control values (weeks 10-12). The migrating myoelectric complex (MMC) was disrupted in only one sheep, and only transiently. In all sheep the frequency of the MMC was increased during infection and there was a progressive inhibition of abomasal, duodenal and jejunal motility. X-radiography showed there was prolonged pooling of digesta in the proximal small intestine which was cleared only at the phase of regular spiking activity. Two sheep given an anthelmintic drench recovered normal motility and clearance of digesta. It is concluded that subclinical infection of sheep with T. colubriformis alters the normal pattern of gastrointestinal motility in the absence of any diarrhoea, and causes inhibition of abomasal and proximal small intestinal motility and digesta flow. The increased frequency of MMCs helps to maintain digesta flow through the proximal small intestine.

Abomasum↗
PubMed1994

Alterations in upper gastrointestinal motility in Helicobacter pylori-positive nonulcer dyspepsia.

OBJECTIVE: To study the association between gastrointestinal motility and Helicobacter pylori (HP) among patients with nonulcer dyspepsia (NUD). METHODS: We examined the gastric emptying and orocecal transit times (OCTT) in patients with NUD who were colonized with Helicobacter pylori (n = 27). NUD was defined as dyspeptic symptoms for at least 3 months in the absence of gastrointestinal pathology as seen on endoscopy and ultrasound. Subjects with diabetes mellitus, thyroid disorder, or abdominal surgery except appendectomy were excluded. The HP-negative patients with NUD (n = 38) served as controls. Solid phase gastric emptying was assessed by radionuclide scintigraphy. OCTT was determined by measuring exhaled breath hydrogen upon administration of lactulose. RESULTS: The two groups were similar with respect to age, sex, race, and history of smoking. Gastric emptying (t1/2) was 64.96 +/- 3.61 min in the HP-negative and 61.0 +/- 6.59 in the HP-positive group (p = NS). The OCTT was 130.9 +/- 17.26 minutes in the HP-negative and 84.28 +/- 11.07 in the HP-positive group (p = 0.03). There was no difference in the prevalence of nonhydrogen producers between the two groups. There was no correlation between gastric emptying and OCTT (p > 0.05). CONCLUSIONS: OCTT is faster among HP-positive patients with NUD than among HP-negative patients. However, gastric emptying is similar in the two groups.

Breath Tests↗
PubMed2005

Maternal steroid enhancement of fetal rabbit gastrointestinal motility.

AIM: The purpose of the present study was to determine the potential maturational effects of maternal dexamethasone administration on fetal upper gastrointestinal motility. METHODS: Nineteen pregnant rabbits were randomized into two groups (DEX and CONT) and studied on either day 24, 27 or 30 of pregnancy (term 31 days). The DEX group received intramuscular dexamethasone (DEX) 2 days before study and the controls received saline. Under ultrasound guidance, a needle was percutaneously inserted into each fetal stomach and fluorescein, labeled with color-coded microspheres, was injected. Two hours later, the length of fluorescein travel throughout the small intestine was measured. The percent motility was calculated by dividing the length of fluorescein travel by the total fetal small intestinal length x 100%. RESULTS: All maternal and fetal rabbits survived. On day 24 the length of fluorescein travel and the percent motility of the DEX group were significantly longer than controls. There were no differences on either day 27 or 30. Fetal growth was significantly suppressed by a single course of DEX at all gestational ages. CONCLUSIONS: Fetal rabbit gastrointestinal motility is significantly increased after prenatal steroids are given early in the last trimester (day 24 of a 31-day gestation). Although beneficial in end-organ maturation, the timing of prenatal steroid administration is crucial to minimize its potential detrimental effects on fetal somatic growth.

Animals↗
PubMed1988

Effects of nutrients on gastrointestinal motility and gastric emptying after Billroth-I gastrectomy in dogs.

We wanted to clarify the way in which nutrients influence gastrointestinal motility and gastric emptying following distal gastrectomy with Billroth-I gastroduodenostomy. Four gastrectomized dogs were equipped with extraluminal strain gauge transducers. Gastric emptying was measured radiographically. Four intact dogs were used as controls for emptying studies. Following gastrectomy, gastric emptying of both acaloric and nutrient meals was rapid in the initial period of the experiments. Gastric outflow was supported by propagating duodenal contractions. Compared with control dogs, the early emptying of nutrient meals was accelerated. In the following period, nutrients markedly slowed gastric emptying compared with acaloric meals due to a segmenting contractile pattern of the duodenum and a significant diminution of gastrointestinal motility. Results suggest that after Billroth-I gastrectomy (1) the control of gastric emptying by nutrients acts too late to slow the initial enhanced gastric outflow, and (2) the duodenal contractile patterns influence gastric emptying.

Animals↗
PubMed1980

[Effects of a new bronchodilator, (alpha RS)-3-formamido-4-hydroxy-alpha-[[[(alpha RS)-p-methoxy-alpha-methylphenethyl] amino] methyl] benzyl alcohol fumarate dihydrate (BD 40A) on gastric acid secretion and gastrointestinal motility (author's transl)].

Effects of a new beta 2-adrenoceptive agonist, BD 40A on gastric acid secretion and gastrointestinal motility were studied in comparison with those of isoproterenol, hexoprenaline and cimetidine. BD 40A (0.3 and 1 microgram/kg i.v.) inhibited dose-dependently gastric acid secretion produced by continuous i.v. infusion of tetragastrin (8 microgram/kg-hr), whereas acid secretion in response to histamine infusion (160 microgram/kg-hr) was resistant to the inhibitory action of BD 40A in pentobarbital anesthetized dogs with gastric pouches. Cimetidine (0.3 and 1 mg/kg) blocked acid secretion induced by either tetragastrin or histamine. When intraduodenally administered to pylorus-ligated rats in a dose of 1 mg/kg, BD 40A and hexoprenaline produced a reduction in acid output. Both drugs (1 microgram/kg i.v.) decreased the amplitude of gastric, duodenal and ileal motility measured by the balloon method in anesthetized dogs. The inhibitory effects of BD 40A on acid secretion induced by tetragastrin and on spontaneous motility of the gastrointestinal tract were antagonized by 1 mg/kg of propranolol. These pharmacological properties of BD 40A were qualitatively similar to those of isoproterenol and may be ascribable to the activation of beta-adrenergic receptors in the gastrointestinal tissue.

Adrenergic beta-Agonists↗
PubMed2006

Comparison of hemodynamic, clinicopathologic, and gastrointestinal motility effects and recovery characteristics of anesthesia with isoflurane and halothane in horses undergoing arthroscopic surgery.

OBJECTIVE: To compare hemodynamic, clinicopathologic, and gastrointestinal motility effects and recovery characteristics of halothane and isoflurane in horses undergoing arthroscopic surgery. ANIMALS: 8 healthy adult horses. PROCEDURE: Anesthesia was maintained with isoflurane or halothane (crossover study). At 6 intervals during anesthesia and surgery, cardiopulmonary variables and related derived values were recorded. Recovery from anesthesia was assessed; gastrointestinal tract motility was subjectively monitored for 72 hours after anesthesia. Horses were administered chromium, and fecal chromium concentration was used to assess intestinal transit time. Venous blood samples were collected for clinicopathologic analyses before and 2, 24, and 48 hours after anesthesia. RESULTS: Compared with halothane-anesthetized horses, cardiac index, oxygen delivery, and heart rate were higher and systemic vascular resistance was lower in isoflurane-anesthetized horses. Mean arterial blood pressure and the dobutamine dose required to maintain blood pressure were similar for both treatments. Duration and quality of recovery from anesthesia did not differ between treatments, although the recovery periods were somewhat shorter with isoflurane. After isoflurane anesthesia, gastrointestinal motility normalized earlier and intestinal transit time of chromium was shorter than that detected after halothane anesthesia. Compared with isoflurane, halothane was associated with increases in serum aspartate transaminase and glutamate dehydrogenase activities, but there were no other important differences in clinicopathologic variables between treatments. CONCLUSIONS AND CLINICAL RELEVANCE: Compared with halothane, isoflurane appears to be associated with better hemodynamic stability during anesthesia, less hepatic and muscle damage, and more rapid return of normal intestinal motility after anesthesia in horses undergoing arthroscopic procedures.

Analysis of Variance↗
PubMed1997

Effects of short-chain fatty acids on gastrointestinal motility.

Besides their action on gut morphology and function, short-chain fatty acids (SCFAs), produced by bacterial fermentation of carbohydrates in the colon, influence gastrointestinal motility. As they are not present in the stomach and proximal small intestine, SCFAs do not directly affect motility of these segments. However, caecal infusion of SCFAs as well as colonic fermentation of lactulose induce a relaxation of the proximal stomach in humans, indicating that SCFAs can affect motility at a distance from their site of production. Moreover, this suggests that SCFAs may be involved in the so-called "ileocolonic brake', i.e. the inhibition of gastric emptying by nutrients reaching the ileo-colonic junction. In the terminal ileum, where their concentration may increase following a colo-ileal reflux, SCFAs stimulate contractions and shorten ileal emptying, which may protect ileal mucosa against the potentially harmful effects of the reflux of colonic contents. Although SCFAs are produced and concentrated in the colon, their action on motility of this organ is not clearly understood and may depend on concentration, molecular structure of the acids, responsiveness of the colonic segments and animal species. The mechanisms of action of SCFAs on gastrointestinal motility are not completely elucidated. They may involve systemic humoral and neural pathways as well as local reflexes and myogenic responses.

Animals↗
PubMed1989

Effect of alpha 2-adrenergic receptor antagonist (midaglizole) on gastrointestinal motility in conscious dogs.

To clarify the physiological role of the mechanism that adrenergic nerve inhibits Ach release from intramural cholinergic nerve endings, the influence of Midaglizole, alpha 2-adrenergic receptor antagonist, to postprandial gastrointestinal motilities in conscious dogs was investigated. Postprandial motilities of gastric antrum, duodenum, ileum, and colon were significantly enhanced by Midaglizole (3.0-5.0 mg/kg body weight, i.v.). These excitatory responses were abolished by atropine (0.05-0.1 mg/kg body weight, i.v.). On the other hand, in most cases (29 cases out of 32), when Midaglizole was administered during quiesent phase of IMC, no change occurred in gastrointestinal motility. However, after subliminal dose of pentagastrin or cisapride, which stimulated Ach release from intramural cholinergic neuron without development of motility, was administered, Midaglizole induced phasic, postprandial motility-like contraction in gastrointestinal tract. Even in the fasted state, when Midaglizole was administered intragastrically, irregular contractions with high amplitude occurred in every regions from gastric antrum to colon. And these excitatory responses were abolished by atropine. Similar reaction was observed also in truncal vagotomized dogs. These results suggest that it is the physiological mechanism that adrenergic nerve presynaptically inhibits Ach release from intramural cholinergic neuron, which is the main mechanism of development of postprandial motility, acting on alpha 2-adrenergic receptor, and has tonic control of postprandial motility.

Adrenergic alpha-Antagonists↗
PubMed1989

Gastrointestinal motility and gastric emptying after Billroth II gastrectomy in dogs.

This study was undertaken to compare the effects of subtotal Billroth II gastrectomy on gastric emptying and gastrointestinal motility with previously published results in intact dogs and in dogs with subtotal Roux-Y gastrectomy. Extraluminal strain gauge transducers were used to study gastrointestinal motility after Billroth II gastrectomy in four conscious dogs. Gastric emptying was measured radiographically. In Billroth II dogs gastric emptying of low-viscosity meals was biphasic with an initial rapid emptying. The addition of nutrients to low-viscosity meals delayed gastric emptying accompanied with reduction in gastric and jejunal motility. Similar to that in Roux-Y dogs, gastric emptying of noncaloric medium-viscosity meals was delayed because of segmenting motor patterns of the jejunal loops, in contrast to the propulsive jejunal motor pattern in intact dogs. Nutrients added to medium-viscosity meals did not change the jejunal motor pattern; gastric emptying was delayed compared with intact dogs. Results show that meal viscosity and jejunal motor pattern influence gastric emptying after Billroth II gastrectomy.

Anastomosis, Roux-en-Y↗
PubMed1994

Therapy of gastrointestinal motility disorders: moving in the right direction.

Coordinated motility of the gastrointestinal tract is responsible for the orderly movement of food and digesta from the mouth to the rectum. This complex series of events results from the integrated activity of enteric nerves, extrinsic nerves, circulating hormones, and smooth muscle. Abnormalities in any of these components or in their integration can result in dysmotility. The important distinction between motility and the transit of luminal contents is emphasized by the recognition that disordered motility may manifest as increased or decreased transit or even as nonpropulsive activity. Similarly, altered motility or transit may or may not be accompanied by alterations in sensation. Ideally, treatment of motility disorders is directed at correction of the underlying pathophysiological defect. Although many of these disorders have been associated with characteristic patterns of abnormal motility, the pathological etiologies involved are poorly understood. Therapy in these cases must then be directed toward amelioration of clinical features and symptoms. The present therapeutic recommendations summarize current modalities in the medical treatment of motility disorders of the esophagus, stomach, small intestine, and colon. Emphasis is given to recent advances in our understanding of motility and to the use of the newer agents in our pharmacological armamentarium.

Esophageal Motility Disorders↗
PubMed1997

Effect of codeine on gastrointestinal motility in relation to CYP2D6 phenotype.

BACKGROUND: Codeine is widely used as an analgesic and antitussive drug. The analgesic effect of codeine is mediated by its metabolite morphine, which is formed by the polymorphically expressed enzyme CYP2D6; therefore poor metabolizers have no analgesia after administration of codeine. Like other opiates, codeine causes a delay of gastric emptying and spastic constipation. It is not yet known whether the effect on gastrointestinal motility is mediated by codeine or its metabolite morphine. METHODS: To test the hypothesis that the metabolite morphine is responsible for the effects of codeine on gastrointestinal motility, a randomized, double-blind, two-way crossover study was performed. The orocecal transit time was studied in five extensive and five poor metabolizers of sparteine with the sulfasalazine-sulfapyridine method, assuming that no effects are observed in poor metabolizers because negligible amounts of morphine are formed. RESULTS: No differences of orocecal transit times were observed between extensive metabolizers and poor metabolizers after oral placebo administration. However, after oral codeine administration orocecal transit time was significantly prolonged in extensive metabolizer but not poor metabolizer subjects. All pharmacokinetic parameters of codeine showed no differences between extensive metabolizers and poor metabolizers. The pharmacokinetic parameters (mean +/- SD) of the metabolite morphine were significantly different between extensive metabolizer and poor metabolizer subjects (peak serum concentration, 13.9 +/- 10.5 versus 0.68 +/- 0.15 pmol/ml; area under the serum concentration-time curve, 27.8 +/- 16.0 versus 1.9 +/- 0.7 hr.pmol/ml; total amount of morphine excreted in urine, 0.160 +/- 0.036 versus 0.015 +/- 0.007 mumol). CONCLUSIONS: Because the orocecal transit time prolongation after codeine administration was observed only in extensive metabolizers, the effect of codeine on gastrointestinal motility, like the analgesia, is mediated by its metabolite morphine.

Analgesics, Opioid↗
PubMed1990

Gallbladder and gastrointestinal motility after hemorrhagic shock.

The alterations in fasting gallbladder and gastrointestinal motility during hemorrhagic shock were investigated. Eight opossums implanted with a gallbladder cannula, gastrointestinal bipolar electrodes, and a carotid catheter were subjected to hemorrhagic shock of 30 mm Hg for 60 minutes by the removal of arterial blood. Shed blood was reinfused after the shock period. Fasting gallbladder volume and gastrointestinal electrical activity were studied before, immediately after, and 24 hours after hemorrhagic shock. Control measurements demonstrated a slow-wave frequency maximal in the duodenum (18.1 +/- 1.1 waves/min), with a plateau in the proximal third of the small bowel, decreasing thereafter. The migrating motor complex (MMC) had a duration of 118 +/- 28 minutes. The average volume of the gallbladder before shock was 5.4 +/- 1.5 ml. Gallbladder volume fluctuated with the MMC, being maximal during phase I and minimal in phase III. The volume of blood removed to reduce mean arterial pressure to 30 mm Hg was 45 +/- 5 ml/kg. Immediately after the shock and blood reinfusion, slow-wave frequency decreased by 40% in the antrum and 25% in the small bowel. The MMC was of shorter duration (91 +/- 22 minutes; p less than 0.05), and gallbladder volume increased to 7.0 +/- 1.7 ml (p less than 0.05). Fluctuations in gallbladder volume during the MMC were absent. Twenty-four hours after shock, slow-wave frequency, MMC, and gallbladder volume had returned to normal and were not different from control measurements. Ischemic damage to the gastrointestinal tract is postulated as the cause of gallbladder dysfunction and altered intestinal motility after hemorrhagic shock.

Animals↗
PubMed2001

Effect of Schistosoma mansoni-induced granulomatous inflammation on murine gastrointestinal motility.

In Schistosoma mansoni-infected mice, gastrointestinal transit was measured in vivo and the neuromuscular function of longitudinal muscle strips of inflamed ileum and noninflamed gastric fundus was assessed in vitro. Eight weeks after infection, the ileal wall was acutely inflamed, as shown by a mucosal inflammatory infiltrate, leading to an increase in mucosal thickness, in myeloperoxidase (MPO) activity, and in interleukin (IL)-1beta production. At that time, both gastrointestinal transit and in vitro ileal contractility were normal. Twelve weeks after infection, chronic granulomatous inflammation led to proliferation of the muscle layer and to a further increase in MPO activity, whereas IL-1beta production normalized. Gastrointestinal transit was decreased, whereas in vitro ileal contractility was increased irrespective of the contractile stimulus. In vitro incubation with IL-1beta (10 ng/ml for 60 min) significantly increased ileal contractility only at 8 wk after infection. Indomethacin, tetrodotoxin, and atropine had no differential effect on ileal contractility in controls and infected mice. In vitro contractility of noninflamed gastric fundus was normal both 8 and 12 wk after infection. We conclude that intestinal schistosomiasis 8 wk after infection is associated only with structural changes of the ileum, whereas 12 wk after infection, both structural and functional changes are present. These changes are characterized by increased ileal wall thickness, decreased gastrointestinal transit, and increased smooth muscle contractility restricted to the inflamed gut segment.

Animals↗