[The autonomic nerves and gastrointestinal motility: interruption of the extrinsic nerves and destruction of the nerves innervating the gastrointestianl wall].
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NK1 and NK3 receptors do not appear to play significant roles in normal GI functions, but both may be involved in defensive or pathological processes. NK1 receptor antagonists are antiemetic, operating via vagal sensory and motor systems, so there is a need to study their effects on other gastro-vagal functions thought to play roles in functional bowel disorders. Interactions between NK1 receptors and enteric nonadrenergic, noncholinergic motorneurones suggest a need to explore the role of this receptor in disrupted colonic motility. NK1 receptor antagonism does not exert consistent analgesic activity in humans, but similar studies have not been carried out against pain of GI origin, where NK1 receptors may have additional influences on mucosal inflammatory or "irritant" processes. NK3 receptors mediate certain disruptions of intestinal motility. The activity may be driven by tachykinins released from intrinsic primary afferent neurones (IPANs), which induce slow EPSP activity in connecting IPANs and hence, a degree of hypersensitivity within the enteric nervous system. The same process is also proposed to increase C-fibre sensitivity, either indirectly or directly. Thus, NK3 receptor antagonists inhibit intestinal nociception via a "peripheral" mechanism that may be intestine-specific. Studies with talnetant and other selective NK3 receptor antagonists are, therefore, revealing an exciting and novel pathway by which pathological changes in intestinal motility and nociception can be induced, suggesting a role for NK3 receptor antagonism in irritable bowel syndrome.
Patients with the irritable bowel syndrome (IBS) often have symptoms from both proximal and distal parts of the gut. Motility disturbances have been reported to occur from the esophagus to the distal colon in IBS patients. The patients often have a decreased lower esophageal sphincter pressure and various abnormalities of esophageal peristalsis. Mean transit time in the small intestine after a meal is short in patients with diarrhoea, and long in patients with constipation and pain compared with normals. IBS patients also show abnormalities of the interdigestive MMC, particularly when exposed to stressful stimuli. Previous studies of the colonic oscillating control potential suggested an increased prevalence of 3/min. slow waves in IBS patients compared with normals, but later studies could not confirm this. Long time measurements with multiple electrodes along the colon show a high prevalence of short-lasting segmental contractions in constipated patients, while both short and long-lasting contractions are decreased in painless diarrhoea. Rectal recordings in IBS patients have shown an increased contractile response up to 3 hrs after a meal. --The disturbed gut motility in IBS patients seems to be due no neural influences rather than strictly myogenic factors.
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The gallbladder and gut should be viewed as hormonally responsive organs the normal physiology of which may be altered by the hormones of pregnancy. The gallbladder enlarges and empties sluggishly in response to meals during pregnancy. Small bowel transit is slowed, and the resting pressure of the lower esophageal sphincter is reduced. All these effects are reversed by delivery; motility reverts toward normal in the postpartum period. The rapid return of normal motility suggests that the effects of pregnancy are hormonally related. Most studies have demonstrated that progesterone, not estrogen, may be the hormone responsible. Although incompletely defined, one mechanism of the effects of pregnancy on motility may be progesterone-induced inhibition of the mobilization of intracellular calcium within smooth muscle cells.
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BACKGROUND: In chronically ill children who refuse to eat, surgery to correct anatomic problems and behavioral treatments to overcome oral aversion often succeed. A few patients fail with standard treatments. The aims of the study were to: 1) investigate motility and gastric sensory abnormalities and 2) describe treatment that was individualized based on pathophysiology in children who failed surgery and behavioral treatments. METHODS: We studied 14 patients (age 1.5-6; mean 2.5; M/F: 7/7). All had a lifelong history of food aversion and retching or vomiting persisting after feeding therapy and fundoplication. All were fed through gastrostomy or gastro-jejunostomy tubes. We studied esophageal and antroduodenal manometry, and gastric volume threshold for retching. We identified when gastric antral contractions were associated with retching and pain. A multidisciplinary treatment program included a variable combination of continuous post-pyloric feedings, drugs to decrease visceral pain, drugs for motility disorders, and behavioral, cognitive, and family therapy. We interviewed parents 2-6 months following testing to evaluate symptoms, mode of feeding and emotional health. RESULTS: We found a motility disorder alone in 2, decreased threshold for retching alone in 5 and both motility and sensory abnormalities in 7. After treatment, 6 of 14 (43%) began eating orally and 80% had improved emotional health. Retching decreased from 15 episodes per day to an average of 1.4 per day (p <0.01). CONCLUSIONS: Upper gastrointestinal motor and/or sensory disorders contributed to reduced quality of life for a majority of children and families with persistent feeding problems. A multidisciplinary approach improved symptoms and problems in these children
AIM: To evaluate the intestinal motility changes evoked by 8 bacterial strains belonging to Bifidobacterium, Lactobacillus and Streptococcus genera within the probiotic preparation VSL#3. METHODS: Ileum and proximal colon segments isolated from guinea-pigs were used as a study model. Entire cells and cell fractions (cell debris, cell wall fraction, cytoplasmatic fraction, proteinaceous and non-proteinaceous cytoplasmatic components) of VSL#3 strains and, as controls, Escherichia coli, Salmonella aboni and Bacillus licheniformis were tested in this in vitro model. RESULTS: Among the bacterial cell fractions tested, only the cytoplasmatic fraction modified intestinal motility. Lactobacillus strains stimulated the contraction of ileum segment, whereas all probiotic strains tested induced proximal colon relaxation response. The non-proteinaceous cytoplasmatic components were responsible for the colon relaxation. CONCLUSION: The results obtained in this study suggest that the proximal colon relaxation activity showed by the probiotic bacteria could be one of the possible mechanisms of action by which probiotics exert their positive effects in regulating intestinal motility.
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Strain gauge recordings of the motility of the antrum, duodenum, and jejunum were made in 10 dogs receiving a daily meal of canned food. Addition of 30 g of either wheat bran, cellulose, or guar gum increased the duration of the postprandial pattern of motility by 41-54% in the duodenum. Only cellulose and gum caused increases in the duration of the postprandial pattern of motility in the jejunum. The normal postprandial pattern of duodenojejunal contractions consisted of bursts of 4-10 rhythmic contractions. When bran or cellulose were added, the bursts were prolonged (12-15 contractions per burst) with 4-15 min intervals between bursts. In contrast, when gum was added, contractions occurred continuously at a rate of 7-8/min, but their amplitude was one-half that seen with the other fibers. The increased number of low amplitude contractions when gum was added caused the postprandial motility index to double. There was no change in the motility index when cellulose was added. Guar gum also increased the frequency of antral contractions by 129%, while bran and cellulose had no effect. Jejunal transit time and flow of digesta were measured in four dogs 2 h after the meal. Addition of bran or gum increased the transit time by 28% and 51%, respectively, but cellulose caused a 900% increase in transit time associated with a 50% reduction in the flow of digesta. Addition of different fibers causes different alterations in postprandial motility. Jejunal transit of digesta appears unrelated to the pattern of contractions.
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The great majority of patients with duodenal ulcer (DU) given a single oral dose (50 mg) of dicetel (pinaverium bromide)--a selective blocker of calcium channels--showed optimization of vegetative reactivity and vegetative support of physical and mental activities. This contributes to relief of psychovegetative syndrome of the modulation of dysfunctions of proximal gastrointestinal tract (GIT). The addition of dicetel to combined treatment of PH shortened healing of DU, relieved pain, stopped gastric and intestinal dyspepsia, corrected motor-tonic defects of the proximal GIT caused by dysfunction of different links of the regulatory-adaptive system.
The effect of intravenous infusion of gastrin II on gastric and colonic motor activity was studied in 12 patients; gastric acid output was also measured. Administration of gastrin at near-maximal dose levels stimulates the motor activity of the antrum but has no measurable effect on the activity of the proximal colon, sigmoid, or rectum. The results suggest that gastrin plays a part in the regulation of gastric motility but that it is not a mediator of the gastro-colic reflex.