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At least 649 records · Page 36Linked to original sources
PubMed1993

Reduced accuracy of 14C-D-xylose breath test for detecting bacterial overgrowth in gastrointestinal motility disorders.

The accuracy of the 14C-D-xylose breath test in the diagnosis of small-bowel bacterial overgrowth was prospectively evaluated in 10 patients with motility disorders: 6 myopathic, 3 neuropathic, and 1 mechanical obstruction. Six of the 10 patients had small-bowel bacterial overgrowth (> or = 10(5) colony-forming units/ml) on culture of small-bowel aspirate. Increased breath 14CO2 levels were documented in three of six patients with positive cultures and in two of four with negative cultures. Two patients with positive results by both methods and one of two patients with positive breath 14CO2 but negative cultures had previously undergone gastric surgery. Three patients with myopathic dysmotility had positive cultures but negative breath tests. Cultures of duodenal aspirates and the D-xylose test had sensitivities of 80% and 40%, respectively, for the finding of hypoalbuminemia. Compared with cultures, the sensitivity and specificity of the breath test were 60% and 40%, respectively. Impaired delivery of 14C-D-xylose for bacterial metabolism may result from postprandial antral hypomotility (n = 4) or low-amplitude (n = 6) small-bowel motility, contributing to the false-negative breath tests. Thus, culture is the optimal method to detect small-bowel bacterial overgrowth in patients with motility disorders.

Adult↗
PubMed1995

Gastrointestinal motility disorders and bacterial overgrowth.

Data on the relationship between small intestinal motility, absorption, and nutrition are sparse and incomplete. Yet, impaired motility is considered to be a plausible cause of bacterial overgrowth, which may have deleterious effects on digestion and absorption. This review discusses the scientific validity and clinical relevance of the concept that intestinal motor abnormalities are responsible for enteric bacterial overgrowth. Disorders associated with intestinal dysmotility and bacterial overgrowth, are illuminated, and concurrent studies of intestinal motility and microflora are focused on in detail. Moreover, practical considerations are given with regard to the clinical management of patients with bacterial overgrowth. Available data allow the conclusion to be drawn that impaired intestinal motility, as evidenced by attenuated migrating motor complex activity, results in bacterial overgrowth. The criteria for an intestinal motility disorder likely to result in bacterial overgrowth have been determined in patients with late radiation enteropathy, but studies in other clinical conditions are needed to establish general guidelines.

Gastrointestinal Diseases↗
PubMed2003

Abnormalities in gastrointestinal motility are associated with diseases of oxidative phosphorylation in children.

OBJECTIVE: Disorders of the mitochondrial electron transport chain enzymes of oxidative phosphorylation (OXPHOS) have neurologic, musculoskeletal, ophthalmologic, cardiac, and GI manifestations. Many adult and pediatric patients with disorders of OXPHOS have abnormalities in intestinal motility. The purpose of this study was to describe pediatric patients who initially presented with signs of GI dysmotility and were later evaluated and found to have a disorder of OXPHOS. METHODS: Data were collected on six patients, including initial GI and neurologic symptoms, histology of skeletal muscle biopsies, mitochondrial DNA mutational analysis, OXPHOS enzyme assay, upper GI barium imaging, technetium-99M liquid gastric emptying scan, upper GI endoscopy, esophageal manometry, and antroduodenal manometry. RESULTS: All six children presented with symptoms of GI dysmotility within 2 wk of life. Patients later developed symptoms of neurologic disorders. All patients had abnormalities in OXPHOS enzyme analysis. Muscle histology showed nonspecific changes with no ragged red fibers. Sequencing of the mitochondrial DNA showed no recognized mutations. No patient had any evidence of intestinal obstruction or malrotation by upper GI barium imaging. Four patients had delayed gastric emptying. Three patients had endoscopic and histologic evidence of esophagitis. All six had demonstrable neuropathic abnormalities by antroduodenal manometry, including the following: nonpropagated antral bursts, absent migrating motor complexes, postprandial antral hypomotility, retrograde migrating motor complexes, and tonic contractions with the migrating motor complex. CONCLUSIONS: Abnormalities in GI motility may be an early presenting sign of disorders of OXPHOS in children.

Age Factors↗
PubMed1983

Neural control of gastrointestinal motility: evidence for noncholinergic regulatory influences.

Although it is well known that neural control of gastric motility occurs via sympathetic, parasympathetic, noncholinergic, and nonadrenergic fibers contained in the vagus nerve, the central sites of origin of these influences are largely unknown. Recent experiments in our laboratory indicate that noncholinergic neural pathways originating in the posterior hypothalamus can markedly influence gastric motility. At least 2 weeks prior to the experiment, mongrel dogs were surgically prepared with bipolar recording electrodes fixed to the serosal surface of the stomach. This prevented violation of the abdominal cavity on the day of testing. Experiments were performed with the animals under alpha-chloralose anesthesia (100 mg kg-1) in temperature-controlled settings. Under stereotactic guidance, bipolar stimulation of the posterior periventricular hypothalamus produced profound reproducible excitatory or inhibitory effects on gastric myoelectric and motor activity. Changes in the frequency and amplitude of pacesetter potentials (PPs) and in the incidence of action potentials associated with them were observed. Stimulation of various loci in 14 dogs resulted in a 71 +/- 7.5% increase in the incidence of action potentials associated with gastric PPs in "excitatory" areas (n = 7) and a 69.1 +/- 4% decrease in this ratio in "inhibitory" areas (n = 19). In general, more lateral stimulation produced greater inhibitory effects. Responses were frequency dependent, with a threshold greater than 25 Hz in most cases. Excitatory gastric responses to hypothalamic stimulation occurred despite full systemic atropinization (0.1 mg kg-1). The physiologic significance of these noncholinergic excitatory pathways influencing distal gastric motility and the neurotransmitters they employ are as yet unknown.

Action Potentials↗
PubMed2001

Effect of hypoxia on fetal rabbit gastrointestinal motility.

During fetal hypoxic stress, blood flow is shunted from nonvital to life-preserving organs, including the heart and brain. Reduced oxygen to the small intestine (SI) induces mucosal injury and may contribute to neonatal necrotizing enterocolitis (NEC). As little is known about the relationship between fetal hypoxia and GI motility, we assessed potential effects in a rabbit model. Twenty-one pregnant rabbits were randomized into two groups, hypoxia (Hyp) and control (Cont). Seven litters were studied at Gestational Days 24, 27, and 30 of their normal 31-day gestation. Under ultrasound guidance each fetal stomach was percutaneously accessed. Fluorescein, labeled with color-coded microspheres for precise fetal identification, was injected. Hyp rabbits breathed 11% oxygen for 1 h after recovery from anesthesia; Cont rabbits breathed room air. Two hours after injection, fetuses were delivered and weighed. The SI was harvested, the length recorded, and the distance fluorescein traveled measured by UV light optical density. Results were analyzed by the unpaired Student test. All injected fetuses (N = 167) survived. The length fluorescein traveled was shorter in Hyp than Cont at all gestational days studied (P < 0.01): Day 24, Hyp = 6.7 +/- 2.0 vs Cont = 8.4 +/- 2.1 cm; Day 27, Hyp = 10.1 +/- 2.9 vs Cont = 19.1 +/- 4.4 cm; and Day 30, Hyp = 16.8 +/- 3.5 vs Cont = 23.1 +/- 5.2 cm. The percentage motility, defined as the length of fluorescein travel divided by total SI length, was also significantly less at all gestational days. Fetal rabbit GI motility was significantly decreased by maternal hypoxia during the last third of gestation. Hypoxia-induced reduction in GI motility may contribute to neonatal NEC.

Animals↗
PubMed1997

Effect of cisapride and renzapride on gastrointestinal motility and plasma motilin concentration in dogs.

The effects of cisapride and renzapride (BRL 24924), on plasma concentration of motilin and gastroduodenal motility were studied in seven dogs with implanted force transducers in the antrum and duodenum. In the interdigestive state, the i.v. administration of cisapride (5 mg) or renzapride (5 mg) administered in phase I resulted in a prompt and marked increase in plasma motilin concentration and in gastroduodenal motility. Mean plasma motilin levels during the first 30 min after cisapride and after renzapride injection were 85.0 +/- 6.5 (+/- S.E.) and 96.1 +/- 6.3 pM., respectively. These values were significantly greater (P < .001) than those for the corresponding time period of the control cycle, 52.2 +/- 5.6 and 57.4 +/- 5.3 pM (mean phase III level, 120 +/- 8.1 pM), respectively. The increases in the motilin level after cisapride or renzapride coincided with significant increases in contractile activities of the antrum to 43.2 +/- 5.3% and 44.9 +/- 4.6% and of the duodenum to 28.4 +/- 3.1% and 34.2 +/- 2.2% of phase III activity (100%) from that in the corresponding control period, 0.7 +/- 0.4% and 0.2 +/- 0.1%, respectively. The changes in both plasma motilin and motility in response to the two drugs were abolished completely by the i.v. administration of atropine. The drugs also enhanced the meal-induced contractile activities of the antrum as well as the duodenum but failed to influence the postprandial plasma motilin concentration. We conclude that cisapride and renzapride have similar effects on plasma motilin and gastroduodenal motility: 1) the two drugs increase plasma motilin levels and stimulate gastroduodenal motility in the interdigestive state, and 2) in the digestive state, both drugs enhance motility without influencing the plasma motilin levels.

Animals↗
PubMed1996

Stimulatory role of the dorsal motor nucleus of the vagus in gastrointestinal motility through myoelectromechanical coordination in cats.

This study was undertaken to investigate the effect of stimulation of the dorsal motor nucleus of the vagus (DMV) on myoelectric activity and motility of the gastric antrum and duodenum in normal and in vagotomized cats. 37 cats were starved for 24 h and then anesthetized with alpha-chloralose (70-80 mg/kg, iv). Electrical stimulation (0.1 mA, 0.2 ms, 50 Hz) of the left DMV was performed through a stereotaxically inserted electrode in 19 of the cats. The remaining 18 cats were injected in the left DMV with a glutamate solution (1 M, 200 nl) through an inserted 3-barreled micropipette. The myoelectric activity (slow wave) and the motility of the gastric antrum (2 cm proximal to the pylorus) and duodenum (3 cm distal to the pylorus) were measured using serosal bipolar electrodes and intraluminal balloons. Both the electrical and the glutamate stimulations of the DMV markedly increased the occurrence of spike potentials on the antral and duodenal myoelectric activity; however, the stimulations significantly decreased the frequency of the antral slow wave. The stimulations also produced increases in the motility of the antrum and duodenum which corresponded to the changes in the myoelectric activity. All the changes in the myoelectric activity and the motility were not observed after the ipsilateral vagotomy. Thus, these results strongly suggest that the dorsal motor nucleus of the vagus has a stimulatory influence on antral and duodenal motility through myoelectromechanical coordination via the vagus nerve in cats.

Animals↗
PubMed1991

[Gastrointestinal motility disorders in diabetes mellitus].

Diabetic patients are prone for the development of autonomic neuropathy with inclusion of the gastro intestinal system. The patients are mainly bothered by disturbances of motility. Depending on the localisation they manifest themselves as constipation or diarrhea. The knowledge of these complications is important, since therapeutic decisions may be influenced.

Constipation↗
PubMed1986

Non-adrenergic non-cholinergic nervous control of gastrointestinal motility patterns.

Non-adrenergic non-cholinergic neurons seem to play an important role in regulation of movements in all parts of the gut. Inhibitory non-adrenergic non-cholinergic neurons mediate a number of descending and ascending reflex effects of physiological and pathophysiological relevance. However, our knowledge in this field is still limited. Development of specific blockers for the non-adrenergic non-cholinergic transmitter substances would help to increase our understanding of gastrointestinal motor functions in health and disease.

Animals↗
PubMed1997

Comparison of effect of mosapride citrate and existing 5-HT4 receptor agonists on gastrointestinal motility in vivo and in vitro.

Mosapride citrate is a new gastroprokinetic agent that enhances the upper GI motility by stimulating 5-hydroxytryptamine4 (5-HT4) receptors. The purpose of this study was to compare the effects of mosapride and the existing 5-HT4 receptor agonists on GI motility in conscious dogs and on various 5-HT4 receptor-mediated responses in vitro. In conscious dogs with force transducers implanted, mosapride (0.3-3 mg/kg i.v.) stimulated the antral motility without affecting the colonic motility. However, cisapride, zacopride and BIMU 8 (0. 1-1 mg/kg i.v.) stimulated both antral and colonic motility. The enhanced GI motility induced by mosapride or cisapride was antagonized by pretreatment with GR113808 (1 mg/kg bolus i.v., thereafter 1 mg/kg/hr infusion), a selective 5-HT4 receptor antagonist. In the receptor binding studies, mosapride inhibited [3H]-GR113808 binding to 5-HT4 receptor sites of guinea pig striatum with an IC50 value of 113 nM. In addition, mosapride caused relaxation of the carbachol-precontracted rat esophagus, enhanced the electrically evoked contractions of guinea pig ileum and evoked the contractions of guinea pig distal colon with EC50 values of 208, 73, and 3029 nM, respectively; this indicates that mosapride has a low affinity for colon than for the rest of the GI tract. In contrast, cisapride, zacopride or BIMU 8 had similar potencies in all preparations examined. In conclusion, these studies indicate that mosapride selectively stimulates upper GI motility in vivo and in vitro. These results also suggest heterogeneity of 5-HT4 receptors in the GI tract.

Animals↗
PubMed1985

Centrally-mediated bombesin effects on gastrointestinal motility.

Administration of bombesin into the lateral cerebral ventricle (i.c.v.) of rats results in a dose-related delay in gastric emptying and small intestinal transit. Recordings of intestinal intraluminal pressure in this species show that the i.c.v. peptide produces a dose-related increase in the frequency of duodenal contractions, and a complex inhibitory/excitatory jejunal effect at low and high doses, respectively. Intrathecal (i.th.) or i.c., but not intraperitoneal (i.p.), bombesin produces a dose-related slowing of gastrointestinal and colonic transit in mice. I.c.v. bombesin is 13.5 and 3406 times more potent in inhibition of gastrointestinal transit than when given by the i.th. or i.p. routes, respectively. Similarly, the i.c.v. peptide is 1.54 and over 11000 times more potent in slowing mouse colonic transit than when given by the i.th. or i.p. routes, respectively. The substance P analogue, D-Arg1, D-Pro2, D-Trp7,9, Leu11-Substance P (DAPTL-SP)(a reported bombesin antagonist in vitro) was not effective in blocking the gastrointestinal transit effects of the peptide in vivo. Transection of the spinal cord at the level of the second thoracic vertebra (T2) eliminates the gastrointestinal and colonic effects of i.th., but not i.c.v. bombesin. Thus, bombesin can affect motor function of the gut via activity within the brain or spinal cord of rats and mice; the activity of the peptide when given at the supraspinal level depends on an intact vagus nerve and adrenal-pituitary axis, while the activity of the peptide given at the spinal level appears to depend on the integrity of ascending spinal-supraspinal pathways.

Animals↗
PubMed2004

Food intake and gastrointestinal motility. A complex interplay.

The complex network between the central nervous system and the enteric nervous system plays a pivotal role in preparing the digestive tract to receive food, process it to activate digestion and control food intake itself. This field has always stimulated researchers and is now receiving notable impetus by the availability of sophisticated technologies able to provide an increasing amount of complex data. This article describes recent findings that underline the role of feeding and the gastrointestinal system in regulating food intake.

Digestion↗