Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GASTROINTESTINAL MOTILITY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,009 records · Page 56Linked to original sources
PubMed2006

Effect of ethanol extract of dried Chinese yam (Dioscorea batatas) flour containing dioscin on gastrointestinal function in rat model.

In this study, a 40% ethanol extract of Chinese yam flour (Dioscoreae rhizoma), containing 177 +/- 58 microg/mL of dioscin, was tested in order to evaluate its pharmacological effects on the gastrointestinal tracts of Sprague-Dawley rats. Via the ingestion of the Chinese yam extract, the secretion of gastric acid was suppressed in the rats, and gastrointestinal motility increased by as much as 10%. The fecal quantity of rats fed on the Chinese yam extract also increased, by more than 40% as compared with that of the controls. The Chinese yam extract was found not to affect the growth of normal intestinal bacteria. However, a great deal of lactose-fermenting bacteria was observed in the fecal samples of rats fed for 6 weeks on 2% Chinese yam extract. This finding would appear to suggest that Chinese yam extract not only induces an improvement in digestive capability, but also affects the conversion of some intestinal flora to helpful bacteria. Our serochemical analyses indicated that serum glucose, neutral lipid, and total cholesterol levels were reduced to some degree by long-term feeding on Chinese yam extract. This finding bolsters the notion that Chinese yam extract may prove helpful as a digestion-aiding agent for patients suffering from hyperglycemia or hyperlipidemia.

Animals↗
PubMed2003

Validation of gastric-emptying scintigraphy of solids and liquids in mice using dedicated animal pinhole scintigraphy.

UNLABELLED: Gastric emptying in small laboratory animals is a useful parameter to assess gastrointestinal motility for physiologic, pharmacologic, or other research purposes. In mice, phenol red recovery is considered the gold standard for determination of gastric emptying. However, this method requires sacrifice of the animal and yields data of gastric emptying at only 1 time point. Gastric-emptying scintigraphy, the gold standard technique in humans, allows sequential and serial measurements in the same subject. In this study, we developed and validated a novel method of gastric-emptying scintigraphy applied in mice, by comparing it with phenol red photospectrometry. METHODS: A dedicated animal pinhole gamma camera was equipped with a specially designed mouse application device. Gastric emptying was measured in unanesthetized mice using pinhole scintigraphy. First, gastric emptying determined with scintigraphy was compared with gastric phenol red recovery simultaneously within the same population. Subsequently, normal values for gastric emptying of solids and liquids in mice were established, and finally, the effects of handling stress and the late effects of frequently used anesthetics or sedatives on gastric emptying were assessed by scintigraphy. RESULTS: Gastric emptying of liquids measured by pinhole scintigraphy did not significantly differ from that measured by phenol red recovery. For the same information, 80% fewer animals were needed for the scintigraphic method. More stress-related delay in gastric emptying was induced by multiple handling of the mice, compared with the less frequent handling that was associated with taking measurements every 10 min or more (P < 0.05). The mean half-emptying time for solids measured by scintigraphy was significantly slower than that for liquid emptying (P < 0.01). Previous anesthesia did not significantly affect gastric emptying 6 h after induction. CONCLUSION: Dedicated small-animal pinhole gastric-emptying scintigraphy is a reliable tool to investigate gastrointestinal motility in mice, significantly reducing the number of laboratory animals needed for statistical power in trials. The technique enables sequential and serial measurement within 1 subject and is thus useful for follow-up investigations, which can be performed even after invasive procedures that require anesthesia.

Analgesics↗
PubMed1994

Colonic transit and anorectal manometry in children with severe brain damage.

OBJECTIVE: This study was conceived to determine the physiologic abnormalities in distal gastrointestinal motility that are responsible for constipation in brain-damaged children. DESIGN: Colonic transit and anorectal manometry were evaluated in 16 children with severe brain damage and constipation (mean age +/- SD; 5.1 +/- 3.5 years) and the results were compared with findings in 15 age- and sex-matched children with functional fecal retention and normal mental development. Anorectal motility findings also were compared with those from 11 asymptomatic children. The progress of radiopaque markers, as determined by sequential plain abdominal radiographs, was used to evaluate segmental colonic transit times. RESULTS: In children with brain damage, colonic transit was prolonged at the level of left colon in 18.8% of the patients, at both left colon and rectum in 56.2%, and at rectum only in 25%. These findings differed (P < .05) from those in children with functional fecal retention wherein transit was prolonged in the left colon and rectum in 20% of the patients and the rectum only in 80%. By anorectal manometry, no significant intergroup differences were detected in anal pressures and in the anorectal motor responses to rectal distention. The rectal compliance in children with severe brain damage was similar to the asymptomatic controls, whereas children with functional fecal retention had increased rectal compliance. CONCLUSIONS: This study shows that colonic transit abnormalities in both the left colon and rectum may be responsible for constipation in children with severe brain damage.

Anal Canal↗
PubMed2006

[Influence of lipopolysaccharide and burn sera on ion channels in smooth muscle cells of colon of guinea pig].

OBJECTIVE: To investigate the influence of lipopolysaccharide (LPS) and burn sera on potassium channels (Kca) in smooth muscle cells of colon of guinea pig so as to elucidate the molecular mechanism of gastrointestinal motility dysfunction after severe burns. METHODS: Single smooth muscle cells were isolated from the taenia coli of guinea pig with enzyme digestion. The standard patch clamp technique was employed to record the single KCa channel currents of smooth muscle cell after challenged by LPS and burn serum. Data were recorded and analyzed by P clamp 6.04 software, and the probability of open (PO), mean open time (OT), mean close time (CT) and current amplitude (CA) were determined. Subsequently, LPS in the concentration of 20, 40, 60, 80 and 100 mg/L, respectively, and normal serum and burn serum in the concentration of 10% were respectively added into medium to examine the influence of the two clamps and sera on the KCa activity. RESULTS: In hyperkalemic solution, the KCa conductance of colonic smooth muscle cells of the guinea pig was (271 +/- 7) pS, indicating it was an ionic channel with high conductivity. Subsequent to depolarization of the membrane, inner-cellular calcium level was increased, and channel PO was also increased, which could be blocked by 1 mmol/L tetraethylammonium (TEA) outside the membrane chaff. As 40 mmol/L TEA inside the membrane chaff did not show such effect, it was proved to be KCa current. The activity of the channel as determined with two kinds of clamps was increased in a dose dependent manner with LPS challenge when the concentration of calcium was 0 mol/L. The KCa activity and PO of the channel was increased obviously when the concentration of LPS was above 40 mg/L (P < 0.05 or 0.01), and it could not be reversed after irrigation with non-LPS medium. By using the two kinds of patch clamps, the KCa were activated by burn sera, but not normal sera. CONCLUSION: Both LPS and burn sera can lead to inhibition of the gastrointestinal motility by activation of KCa channels.

Animals↗
PubMedDate not supplied

IL-9 enhances growth of ICC, maintains network structure and strengthens rhythmicity of contraction in culture.

Interstitial cells of Cajal (ICC) play a critical role in the control of gastrointestinal motility as pacemaker cells and as regulators of enteric innervation. ICC are one of the first cell types that are injured during an inflammatory process and maintenance of ICC health or promotion of growth and development maybe crucial in recovery after injury. The aim of this study was to evaluate the role of IL-9 in the growth, development and maintenance of ICC in culture. IL-9 in concentrations from 0.02 to 1 microg/ml promoted individual ICC growth and maintenance of the ICC network structure inside tissue explants under culture conditions. The number of ICC grown out of the explants increased significantly at day 4 of culture in the presence of 0.02, 0.5 and 1 microg/ml IL-9. In the presence of 0.5 microg/ml IL-9, explants in culture maintained a higher frequency and stabilized the frequency of spontaneous contractile activity. The ultrastructure of the ICC after 4 days in culture was similar to that in situ. Our data indicate that IL-9 promotes ICC growth in culture and it can be hypothesized that IL-9 is a critical factor in the maintenance of ICC health and ICC repair after injury.

Animals↗
PubMed2000

Interstitial cells of cajal and inflammation-induced motor dysfunction in the mouse small intestine.

BACKGROUND & AIMS: Interstitial cells of Cajal (ICC) play an important role in the control of gastrointestinal motility. We aimed to determine a potential role for ICC in the pathophysiology of inflammation-induced motor disorders. METHODS: Effects of Trichinella spiralis infection on electrical pacemaker activity, the structure of ICC associated with Auerbach's plexus, and in vivo motor patterns were studied in the mouse small intestine. RESULTS: Between days 1 and 15 after infection, structural damage occurred in the network of ICC, particularly in the processes connecting ICC to each other and to smooth muscle cells. This was associated with desynchronization of electrical pacemaker activity. Abnormal slow wave activity occurred, including doubling of frequency and electrical quiescence, leading to the development of ectopic pacemaker activity in vivo. In vivo motor patterns in the small intestine changed from consistent peristaltic contractile activity in control animals to periods of quiescence alternating with both orally and aborally propagating contractile activity in the presence of inflammation. Sixty days after infection, all parameters studied had returned to normal values. CONCLUSIONS: Inflammation-induced alterations in the network of ICC of the small intestine associated with Auerbach's plexus lead to disorganization of motor patterns. Because of the strong temporal correlation between damage to the ICC network, electrical uncoupling, the appearance of ectopic pacemaker activity, and the occurrence of retrograde peristalsis, it is concluded that ICC can play a major role in inflammation-induced motor disturbances.

Animals↗
PubMed2005

CRF-induced calcium signaling in guinea pig small intestine myenteric neurons involves CRF-1 receptors and activation of voltage-sensitive calcium channels.

Corticotropin-releasing factor (CRF) is a 41-amino acid peptide with distinct effects on gastrointestinal motility involving both CRF-1 and CRF-2 receptor-mediated mechanisms that are generally claimed to be centrally mediated. Evidence for a direct peripheral effect is rather limited. Electrophysiological studies showed a cAMP-dependent prolonged depolarization of guinea pig myenteric neurons on application of CRF. The current study aimed to test the direct effect of CRF on myenteric neurons and to identify the receptor subtype and the possible mechanisms involved. Longitudinal muscle myenteric plexus preparations and myenteric neuron cultures of guinea pig small intestine were incubated with the calcium indicator Fluo-4. Confocal Ca(2+) imaging was used to visualize activation of neurons on application of CRF. All in situ experiments were performed in the presence of nicardipine 10(-6) M to reduce tissue movement. Images were analyzed using Scion image and a specifically developed macro to correct for residual minimal movements. A 75 mM K(+)-Krebs solution identified 1,076 neurons in 46 myenteric ganglia (16 animals). Administration of CRF 10(-6) M and CRF 10(-7) M during 30 s induced a Ca(2+) response in 22.4% of the myenteric neurons (n = 303). Responses were completely abolished in the presence of the nonselective CRF antagonist astressin (n = 55). The selective CRF-1 receptor antagonist CP 154,526 (n = 187) reduced the response significantly to 2.1%. Stresscopin, a CRF-2 receptor agonist, could not activate neurons at 10(-7) M, and its effect at 10(-6) M (15.3%, n = 59) was completely blocked by CP 154,526. TTX 10(-6) M (n = 70) could not block the CRF-induced Ca(2+) transients but reduced the amplitude of the signals significantly. Removal of extracellular Ca(2+) blocked all responses to CRF (n = 47). L-type channels did not contribute to the CRF-induced Ca(2+) transients. Blocking N- or P/Q-type Ca(2+) channels did not reduce the responses significantly. Combined L- and R-type Ca(2+) channel blocking (SNX-482 10(-8) M, n = 64) abolished nearly all responses in situ. Combined L-, N-, and P/Q-type channel blocking also significantly reduced the response to 8.6%. Immunohistochemical staining for CRF-1 receptors clearly labeled individual cell bodies in the ganglia, whereas the CRF-2 receptor staining was barely above background. CRF induces Ca(2+) transients in myenteric neurons via a CRF-1 receptor-dependent mechanism. These Ca(2+) transients highly depend on somatic calcium influx through voltage-operated Ca(2+) channels, in particular R-type channels. Action potential firing through voltage-sensitive sodium channels increases the amplitude of the Ca(2+) signals. Besides centrally mediated effects, CRF is likely to modulate gastrointestinal motility on the myenteric neuronal level.

Animals↗
PubMed1999

Acquired motility disorders in childhood.

Acquired motility disorders in childhood cause a number of gastrointestinal symptoms - principally, recurrent vomiting, abdominal pain and distension, constipation and loose stools. Gastrointestinal motility disorders result from disturbances of the control mechanisms of gut motor activity, which may be produced by organic disease involving enteric nerves and muscle, perturbation of the humoral environment of the nerves and muscle, and altered central nervous system input. In children, both congenital and acquired disease processes may produce these pathogenetic mechanisms, resulting in syndromes that vary in severity from chronic intestinal pseudo-obstruction to the irritable bowel syndrome.

Animals↗
PubMed1990

Where do we stand on gastric motility?

This review deals with several aspects of gastrointestinal motility. It attempts to relate basic knowledge to clinically relevant issues. The review is organized around specific contractile patterns and tasks in the gastrointestinal region that are grouped into three broad categories: tonic contractility of the stomach, antral phasic contractility, and resistance of the gastric outlet. There is also a section dealing with the evaluation of gastric motor function for diagnostic purposes describing the technologic means for investigating motility disorders in patients presenting with different clinical syndromes. In this section there is also reference to the criteria to be used in interpretation of the results and practical advice on the use of each test. Finally, the review deals with the issue of treatment of gastric motor disorders, comprising both dietary and pharmacologic approaches.

Gastric Emptying↗
PubMedDate not supplied

AS-4370, a novel gastrokinetic agent free of dopamine D2 receptor antagonist properties.

The gastrokinetic effects of AS-4370, 4-amino-5-chloro-2-ethoxy-N-([4-(4-fluorobenzyl)-2-morpholinyl] methyl) benzamide citrate, were compared with those of metoclopramide in experimental animals. In rats, AS-4370 increased the gastric emptying of a semi-solid meal and of resin pellets at dose ranges of 0.03-30 mg/kg and 1-10 mg/kg p.o., respectively. The minimal effective doses were 3-10 times lower than those of metoclopramide. Gastric emptying, delayed by gastroduodenal surgical intervention, was improved with AS-4370 (0.3-3 mg/kg p.o.). In conscious dogs with strain gauges implanted, AS-4370 (0.5 and 1.0 mg/kg i.v.) enhanced antral and duodenal motility without affecting ileal and colonic motility, indicating a selective enhancing effect on upper gastrointestinal motility. AS-4370 (10(-7) - 3 x 10(-5) M) increased electrically evoked, cholinergically mediated contractions in isolated guinea-pig ileum. AS-4370 (3 mg/kg i.v.) was without effect on gastric acid secretion in anesthetized rats. Unlike metoclopramide, AS-4370 neither depressed the active avoidance response in mice nor the food-reinforced lever pressing response in rats, even at 100 mg/kg p.o. Moreover, AS-4370 (10(-4) M) showed no affinity for D2, alpha 1, alpha 2, 5-HT1 and 5-HT2 binding sites in rat brain synaptic membranes. These results suggest that AS-4370 is a new and potent gastrokinetic agent that lacks dopamine D2 receptor antagonist properties.

Animals↗
PubMed1989

Motility malfunction of the gastrointestinal tract by rare diseases--fibrosis of the intestinal wall.

We report on two children who were admitted with chronic ileus without mechanical obstruction. In the 4-month-old female newborn, high-dose radiation was applied after extirpation of a sympathicoblastoma. Within a few years a metaplasia of the muscle coat of the small intestine developed with a resulting malabsorption syndrome. Although the damaged part of the intestine was resected, the process progressed and the child died. In the second case, a chronic ileus developed at the age of 10 years as a result of fibrosis of the intestinal tract. Repeated laparotomies were performed, and no mechanical obstruction could be found. The most probable diagnosis is a form of scleroderma affecting mainly the alimentary tract without any skin involvement. The patient died in a severe cachexia.

Child↗
PubMed1999

Evaluation of small-bowel transit for solid and liquid test meal in healthy men and women.

Evaluation of severe functional gastrointestinal motility disorders requires an investigation of the entire gastrointestinal tract. This should be possible with a single radionuclide imaging study. The purpose of this study was (1) to define normal values of small-bowel transit in men and women and (2) to assess a possible difference between gender or test meal, since it has been shown that women have slower gastric emptying than men, and gastric emptying of solids is slower than liquids. A standard gastric-emptying test for a solid (technetium-99m sulphur colloid, 230 Kcal) and liquid (indium-111 DTPA water) test meal was performed in 12 healthy male and 12 healthy female volunteers. After 135 min, the volunteer was placed in the supine position for static imaging of the abdomen every 15 min for 6 h. Decay and crossover-corrected geometric mean gastric-emptying data were fit to a modified power exponential function to determine the 10% stomach emptying time for solids and liquids separately. An ROI was drawn around the caecum and ascending colon to determine the arrival time of at least 10% of the solid and liquid test meal. Ten percent small-bowel transit time (10% SBTT) and orocaecal transit time (OCTT) were calculated. The OCTT for males and females, respectively for solids and liquids, are 294.6 +/- 18.8; 301.3 +/- 24.5; 294.6 +/- 18.8 and 301.3 +/- 24.5 min. The 10% SBTT for males and females, respectively for solids and liquids, are 280.3 +/- 18.4; 280.6 +/- 24.0; 288.2 +/- 18.9 and 297.4 +/- 24.4 (mean +/- SEM) min. We observed a simultaneous transfer of solids and liquids from the terminal ileum to caecum (correlation coefficient 0.90). There is no statistically significant difference in SBTT between gender or solids and liquids. In contrast to the gastric-emptying time, the SBTT of solids and liquids were not significantly different nor was a gender difference found. Determination of the OCTT seems to be the simplest and most accurate approach to measure SBTT. Since ileocaecal transfer occurs as a bolus phenomenon, a 111In-labelled test meal can also be used for the determination of colon transit in a single imaging study protocol.

Adult↗
PubMed2002

Interstitial cells of Cajal, enteric neurons, and smooth muscle and myoid cells of the murine gastrointestinal tract express full-length dystrophin.

A gene located on the X chromosome is responsible for the transcription of several mRNA and related dystrophin isoforms. Lack or truncated expression of the 427-kDa, full-length isoform in skeletal muscle results in Duchenne muscular dystrophy (DMD). Patients with DMD, as well as mdx mice, a mutant strain also lacking this isoform, show gastrointestinal dismotilities. The present aim was to identify the cell types that express full-length dystrophin in the gastrointestinal tract. An immunohistochemical study was performed using an antibody specific for this isoform, and double labelings were made for interstitial cells of Cajal (ICC) identification and to verify whether all neurons express full-length dystrophin. Three different fixation procedures were used. The results showed that ICC, enteric neurons, and smooth muscle and myoid cells expressed full-length dystrophin. In ICC and neurons, dystrophin-immunoreactive patches were irregularly distributed at the cell contour and within the cytoplasm. In smooth muscle and myoid cells, regularly spaced dystrophin-immunoreactive bars were located along the cell contour. Labeling intensity varied according to fixation procedure. The different subcellular distributions of dystrophin immunoreactivity might reflect diverse roles played by full-length isoforms in each cell type. Dystrophin loss in cells involved in gastrointestinal motility might explain the gastrointestinal symptomatology affecting DMD patients and mdx mice.

Animals↗
PubMed1993

Prostaglandin E2 stimulation of acetylcholine release from guinea pig myenteric plexus neurons.

Prostaglandins are widely distributed within the gastrointestinal tract and have important effects on gastrointestinal motility. Although actions upon gastrointestinal smooth muscle have been demonstrated for prostaglandins (PG), neural mechanisms may also be important. The effects of PGE2 on acetylcholine (ACh) release were studied using guinea pig myenteric plexus neurons in primary culture. PGE stimulated the release of ACh in a dose-dependent manner, with a median effective dose (ED50) of 0.8 x 10(-6) M. Involvement of L-type calcium channels was implied by the sensitivity of PGE2-stimulated ACh release to omega conotoxin or diltiazem. In addition, ACh release stimulated by PGE2 could be inhibited by co-incubation with dideoxyadenosine or Rp-cAMPS, agents that act upon cyclic adenosine monophosphate (cAMP)-dependent signaling pathways. PGE2 has direct effects upon myenteric neurons to stimulate cholinergic transmission.

Acetylcholine↗
PubMed1999

Comparison of tegaserod (HTF 919) and its main human metabolite with cisapride and erythromycin on cardiac repolarization in the isolated rabbit heart.

Tegaserod (HTF 919) is a new drug being developed for gastrointestinal motility disorders. Because other gastrointestinal prokinetic agents, such as cisapride and erythromycin, cause slowing of cardiac repolarization and have been implicated in the development of the potentially fatal ventricular arrhythmia, torsades de pointes, a study was initiated to determine whether tegaserod and its main human metabolite adversely influence cardiac repolarization. By using isolated Langendorff-perfused rabbit hearts, we show that QT intervals remain unchanged at concentrations of tegaserod from 0.5 to 10 microM. It was not until the tegaserod concentration was increased to 50 microM (roughly 500-5,000 times more concentrated than those typically found in human plasma after administration of recommended clinical dosages), that a small, but significant increase in the QT interval (12+/-4%; p < 0.05; n = 4) was observed. No significant changes in QT occurred in the presence of the tegaserod metabolite at any of the concentrations tested (0.5-50 microM). In contrast, cisapride caused QT lengthening at concentrations as low as 0.1 microM, with significant QT increases occurring when 5-50 microM cisapride was used (22+/-4% to >70%, respectively; p < 0.01; n = 4). Erythromycin also caused significant lengthening of QT intervals (11+/-2%; p < 0.001; n = 4), although 100 microM concentrations of this drug were required to achieve this effect. These results demonstrate that both cisapride and erythromycin can slow cardiac repolarization at therapeutic doses and that tegaserod's lack of QT prolongation at therapeutic doses suggests that it has the potential to be a safer alternative to cisapride as a gastrointestinal prokinetic agent.

Animals↗
PubMed2004

Mechanisms of postoperative ileus.

Postoperative ileus is an iatrogenic condition that follows abdominal surgery. Three main mechanisms are involved in its causation, namely neurogenic, inflammatory and pharmacological mechanisms. In the acute postoperative phase, mainly spinal and supraspinal adrenergic and non-adrenergic pathways are activated. Recent studies, however, show that the prolonged phase of postoperative ileus is caused by an enteric molecular inflammatory response and the subsequent recruitment of leucocytes into the muscularis of the intestinal segments manipulated during surgery. This inflammation impairs local neuromuscular function and activates neurogenic inhibitory pathways, inhibiting motility of the entire gastrointestinal tract. The mechanisms underlying the recruitment of the inflammatory cells, and their interaction with the intestinal afferent innervation, are discussed. Finally, opioids administered for postoperative pain control also contribute to a large extent to the reduction in propulsive gastrointestinal motility observed after abdominal surgery.

Analgesics, Opioid↗