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At least 397 records · Page 22Linked to original sources

PubMed1988

Gastrointestinal motility: some basic concepts.

The spatial and temporal patterns of phasic contractions in the gastrointestinal tract are regulated by a complex interplay between the myogenic, neural and chemical control mechanisms. These contractions are largely responsible for the mixing and propulsive movements of the gut after a meal. In the fasted state, organized groups of contractions called cyclic motor activity and migrating motor complex keep the upper digestive tract clean of residual food and debris. In addition, the small intestine and the colon generate giant migrating contractions which are several-fold stronger than the postprandial phasic contractions and migrate uninterrupted over long distances. The giant migrating contractions are effective in rapid propulsion. The upper small intestine and the antrum generate retrograde giant contractions that generally precede vomiting.

Animals↗

PubMed2006

Ontogeny of excitatory and inhibitory control of gastrointestinal motility in the African clawed frog, Xenopus laevis.

The transparent body wall of Xenopus laevis larvae during the first developmental stages allows in vivo studies of gastrointestinal tract activity. The purpose of this study was to chart the ontogeny of gut motility in Xenopus larvae and to identify the most important control systems during the first developmental stages. Coordinated descending contraction waves first occurred in the gut at Nieuwkoop and Faber stage 43 [0.8 +/- 0.1 contractions/min (cpm)] and increased to 4.9 +/- 0.1 cpm at stage 47. The cholinergic receptor agonist carbachol (5-10 microM) increased contraction frequency already at stage 43, as did neurokinin A (NKA, 0.3-1 microM). The muscarinic antagonist atropine (100 microM) first affected contraction frequency at stage 45, which coincides with the onset of feeding. The tachykinin antagonist MEN-10,376 (6 microM) blocked NKA-induced contractions but not spontaneous motility. Both sodium nitroprusside [nitric oxide (NO) donor, 1-10 microM] and vasoactive intestinal peptide (VIP, 0.1-1 microM) inhibited contractions from the earliest stage onward. Blocking NO synthesis using NG-nitro-L-arginine methyl ester (100 microM) had no effect per se, but antagonized VIP evoked inhibition at stage 47. We conclude that gastrointestinal motility is well developed in the Xenopus laevis larvae before the onset of feeding. Functional muscarinic and tachykinin receptors are present already at the onset of motility, whereas a cholinergic tone develops around the onset of feeding. No endogenous tachykinin tone was found. Functional VIP receptors mediate inhibition at the onset of motility. NO seems to mediate the VIP effect at later stages.

Animals↗

PubMed1985

The detection and evaluation of drug-induced changes in the gastrointestinal motility of beagle dogs using a 111In-labelled resin mixed into a standard meal as tracer.

An investigation was performed to establish the usefulness of 111In-labelled polymer beads mixed into a standard meal as a tracer of gastrointestinal(GI)-motility changes due to the influence of various drugs. The labelled polymer beads were well mixed into the food, which was then fed to healthy beagle dogs undergoing drug therapy. GI motility was monitored using a gamma camera and data processor. The results were compared to those obtained from corresponding placebo studies on the same dogs. A significant acceleration of gastric emptying and colon transit was noted under the influence of a gastric and intestinal prokinetic coded R51619. No influence on GI motility could, however, be detected after the administration of a calcium-blocking agent to the dogs.

Animal Feed↗

PubMed1993

Stimulation of gastrointestinal motility by cisplatin in the ferret: activation of an intrinsic cholinergic mechanism dissociated from emesis.

Motility was recorded from the corpus, antrum and small intestine of the urethane anaesthetised ferret. The gastrointestinal effects of the highly emetic cytotoxic anticancer agent, cisplatin were investigated following intravenous administration (10 mg/kg i.v.). Following injection, cisplatin induced a prompt onset (< 2 min) increase in motility (tone and contraction amplitude) in all regions with a duration of < 15 min. Acute vagotomy did not abolish the effect but reduced the peak amplitude in the antrum only. Chronic subdiaphragmatic vagotomy significantly enhanced the cisplatin-induced rise in tone in the corpus, the contraction amplitude in the antrum and the duration of the response in the duodenum. The stimulatory effect of cisplatin was blocked in all regions by atropine but not naloxone or the 5-HT3 receptor antagonist ondansetron. This study reports a previously undescribed gastrointestinal motility effect of cisplatin in vivo that is temporally dissociated from emesis. It is proposed that the results provide evidence for a neuroactive effect of cisplatin on enteric cholinergic neurones.

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PubMed1951