[Regulation of gastrointestinal motility by gastrointestinal hormones (author's transl)].
Explore the source record for details and available documents.
Animals↗
SEARCH · PubMed Health
Results for “Gastrointestinal Motility”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Gastrointestinal motility and gastrointestinal hormones].
Explore the source record for details and available documents.
Animals↗
Effects of a new 1,4-dihydropyridine, lacidipine, on gastrointestinal motility and other gastrointestinal functions.
Lacidipine is a new 1,4-dihydropyridine calcium entry blocker endowed with slow onset of action and potent and long-lasting antihypertensive activity. This study investigated the effect of lacidipine on some gastrointestinal functions, mainly gastrointestinal motility, in rats and dogs. In fasting conscious dogs chronically fitted with electrodes and strain gauges along the small bowel, lacidipine (12 micrograms/kg i.v. bolus or 10 micrograms/kg/h for 3 h) did not modify the migrating motor complex pattern or intestinal spike activity. In the rat, lacidipine proved less active (ED 50 greater than 100 mg/kg p.o.) than nitrendipine (ED 50 = 31 mg/kg p.o.) in inhibiting gastric emptying of a liquid meal, whereas the opposite was true after a solid meal (ED 50 = 10.9 and 35.0 mg/kg p.o., respectively). Lacidipine inhibited fecal pellet output at lower doses (ED 50 = 14.8 mg/kg p.o.) than nitrendipine (ED 50 = 40.1 mg/kg p.o.). On histamine-induced gastric acid secretion, the effect of 100 micrograms/kg i.v. lacidipine was moderate (maximum inhibition 45%). The gastrointestinal effects displayed by lacidipine appear at doses at least 5 and 50 times as high as those affecting blood pressure after intravenous and oral administration, respectively. Thus, lacidipine is unlikely to cause noteworthy unwanted effects on the gastrointestinal tract.
Animals↗
Psychogenic vomiting--a disorder of gastrointestinal motility?
Explore the source record for details and available documents.
Gastrointestinal Motility↗
Role of fasting gastrointestinal motility in the variability of gastrointestinal transit time assessed by hydrogen breath test.
Gastrointestinal motility and transit time, measured by the hydrogen breath test, were simultaneously assessed in six healthy volunteers. Each subject underwent six studies on separate days. On each day motility was measured in the gastric antrum, duodenum, and proximal jejunum and 15 g of lactulose was given either by mouth during gastric phases I, II, III of the motor migrating complex or infused duodenally during duodenal phases I, II, III, one phase being studied each day in random order. Fasting activity was not interrupted by the lactulose. The lactulose transit time decreased significantly from a peak with phase I through phase II to a minimum with phase III (mean (SD) 155 (26) min v 120 (10) min v 94 (14) min, p less than 0.001). Similar results were noted when the lactulose was instilled intraduodenally (156 (23) min v 125 (19) min v 100 (17) min, p less than 0.001). No correlation was found between motility index and transit. These results suggest that different phases of fasting gastrointestinal motility are major determinants of the transit time estimated by the hydrogen breath test and explain the variability of this test in practice.
Administration, Oral↗
Extrinsic neural influences on gastrointestinal motility.
The gastrointestinal tract is capable of carrying on all its major functions after all extrinsic nerves have been cut. This automaticity is due to the local nervous mechanisms in the walls of the gastrointestinal tract and the inherent properties of the smooth muscles in its walls, and gastrointestinal hormones. All levels of the central nervous system have been shown, by stimulation and ablation studies, to influence the motility of the entire gastrointestinal tract. Throughout many cerebral areas there are loci which, on stimulation, exert both inhibitory, and less often, excitatory influence on gastrointestinal motility. These influences are mediated by sympathetic and parasympathetic visceral efferent nerves, as well as humoral agents from the neurohypophysis. Thus, they impose an influence of higher control on the automatically efficient intrinsic motility. They are guided by information received from visceral, cranial, and somatic afferents, as well as intracerebral, or psychic inputs. Under normal circumstances they only influence gastrointestinal activity as will best afford the optimal functioning of a performance done automatically with efficiency and finesse.
Afferent Pathways↗
[Central regulation of gastrointestinal motility and secretion].
Gastrointestinal motility and secretions are regulated by cerebral nuclei via autonomic efferents in a coordinated fashion. At rest, vagal activity dominates while during different forms of stress the activated sympathetic nervous system markedly modulates secretions and motility. Expression of unique neuropeptides in distinct CNS regions facilitates the differentiated regulation of visceral functions. For example, corticotropin-releasing factor regulates the homeostatic pattern of visceral functions during stress. Furthermore, thyrotropin-releasing hormone accounts for parasympathetic activity while calcitonin gene related peptide predominantly accounts for sympathetic modulation of gastrointestinal motility and secretions. These neuropeptides coordinate visceral functions producing integrated motor and secretory responses that facilitate diverse digestive processes.
Animals↗
Bile acid malabsorption caused by gastrointestinal motility dysfunction? An investigation of gastrointestinal disturbances in familial amyloidosis with polyneuropathy.
Gastrointestinal dysfunction due to autonomous neuropathy is a complication described in various diseases such as diabetes mellitus, multiple sclerosis, and familial amyloidosis with polyneuropathy. We present the results of a prospective investigation of bile acid malabsorption in 17 patients with familial amyloidosis by means of 75Se-labelled homocholic-tauro acid (SeHCAT). The diagnosis was in all cases verified by the DNA test for mutation of transthyretin in position 30. Small-intestinal biopsy specimens were examined for deposits of amyloid, and the presence of gastric retention was evaluated by gastroscopy. In addition, the patients were investigated for bacterial overgrowth by means of the bile acid breath test (BABT). A high frequency of abnormal BABT results (44%) was encountered. However, 65% also had abnormal low SeHCAT values, indicating bile acid malabsorption. Only two patients had abnormal BABT and normal SeHCAT results, indicating bacterial contamination of the small intestine. Bile acid losses increased with the duration of gastrointestinal symptoms. Significantly lower SeHCAT values were encountered in patients with gastric retention, whereas the occurrence of amyloid deposits in small-intestinal biopsy specimens was without effect on SeHCAT retention. Bile acid malabsorption is frequently encountered in familial amyloidosis with polyneuropathy and seems to be more closely associated with gastrointestinal motility dysfunction than with amyloid deposits in the intestinal mucosa.
Amyloidosis↗
Comparison of the effects of midecamycin acetate and clarithromycin on gastrointestinal motility in man.
The gastrointestinal motor effects of the macrolide antibiotic, clarithromycin, were compared with those of midecamycin acetate. The method of investigation consisted of intraluminal pressure measurements in the gastric antrum and upper small intestine by means of a low compliance perfused catheter system. Six healthy volunteers participated in the single-blind, placebo-controlled study of both interdigestive and postprandial gastrointestinal motility. Clarithromycin was administered by mouth in a dose of 250 mg b.i.d.; midecamycin acetate was given in a dose of 600 mg b.i.d. The effect of midecamycin acetate on gastric antral and jejunal motility was not significantly different from that of placebo. This was true for both the interdigestive and the postprandial phases of gastrointestinal motility. Oral treatment with clarithromycin (250 mg, b.i.d.) resulted in a statistically significant increase in the postprandial number of antral contractions per hour as well as in the postprandial antral motility index, as compared to placebo.
Adult↗
Experimental gastrointestinal motility: where to go.
Gastrointestinal motility is a major field of research. However, despite a huge amount of data available in the literature, its exact role has yet to be defined. This paper deals with the choice of animal research models for motility studies.
Animals↗
Influence of sulpiride on gastrointestinal motility: experimental radiological study in the dog.
A radiological study has been carried out in the dog to control the influence of N-ethyl-2(2-methoxy-5-sulfamido-benzamidomethyl)-pyrrolidine (sulpiride) on the motility of the gastrointestinal tract. The drug was administered orally and parenterally at different doses for each pharmaceutical form and for such route of doses for each pharmaceutical form and for each route of administration. In doses which were considered optimal, the results have demonstrated that sulpiride exerts hypertonic and hyperphasic effects on the smooth musculature of the gastrointestinal tract. Consequently, there is a reduction of the transit time and of the emptying of the opaque meal in the various sectors of the gastrointestinal tract, which is in the order of about 50% with respect to normal. Using doses which are inferior to those considered optimal, no significant results were obtained, while following higher doses the action of sulpiride is manifested by an inhibitory effect on gastrointestinal motility.
Administration, Oral↗
[An experimental study of gastrointestinal motility during chronic large bowel obstruction].
Gastrointestinal motility and plasma PYY levels were investigated under chronic progressive large bowel obstruction in dogs. The obstruction device was applied around the descending colon at a laparotomy and gastrointestinal motility was recorded with strain gauge force transducers in the conscious state. Complete obstruction occurred at 26 days (21-33 days). The duration of postprandial interruption of motor complex (DIMC) in the antrum and duodenum were prolonged progressively, at partial obstruction (17.7 +/- 2.7 hr; p less than 0.05) and complete obstruction (23.0 +/- 4.0 hr; p less than 0.01) vs in control (13.7 +/- 1.9 hr), while DIMC in the small bowel showed no significant changes. Progressive obstruction caused hypermotility in the proximal colon to the obstruction and hypomotility in the distal colon. These dysmotility were improved after resection of the obstructed segment and anastomosis. Plasma PYY levels in the fasting state showed no significant increase at complete obstruction (42.6 +/- 14.5 pmol/l) vs in control (32.9 +/- 10.2 pmol/l).
Animals↗
[Gastrointestinal motility and autonomic nerve dysfunction].
Gastrointestinal motility is greatly influenced by both the autonomic nervous system (ANS) and the enteric nervous system (ENS). Dysfunction of ANS and/or ENS produces various kinds of dysmotility from the esophagus to the colon. Generalized autonomic dysfunction, often seen in diabetics, causes abnormal peristaltic waves in the esophagus, abnormal electrical activity of the stomach, delayed gastric emptying and delayed intestinal transit. Localized disorders of the enteric nervous system is seen in patients with achalasia and Hirschsprung's diseases. Functional disorders, without evidence of organic disorders, like non-cardiac chest pain, non-ulcer dyspepsia, irritable bowel syndrome, can be partly caused by abnormal function of autonomic nervous system.
Autonomic Nervous System↗
[The effects of flavoxate hydrochloride on the gastrointestinal motility (author's transl)].
The experiments were performed to study the effects of Flavoxate hydrochloride on the gastrointestinal motility and its underlying mechanism. Gastrointestinal motility was inhibited at first and then accelerated markedly after the intravenous injection of Flavoxate hydrochloride (10 mg/kg) in the experiments of anesthetized dogs. For analyzing the underlying mechanism of this response the following experiments were executed. 1) The pendular movements of isolated ileum of rabbits were accelerated with administration of low concentration of Flavoxate hydrochloride less than 10(5) g/ml, while these were reduced with administration of high concentration more than 10(4) g/ml. Because the tetrodotoxin (2.5 times 10(7) g/ml) has no essential effect on these responses, it could be postulated that Flavoxate hydrochloride has direct effect on intestinal smooth muscle itself. 2) Flavoxate hydrochloride (10 mg/kg) induced the differentiated regional response of the sympathetic outflow, that is, the parallel decrease of cutaneous and cardiac sympathetic activities, and the converse increase of splanchnic activity. Therefore, Flavoxate hydrochloride is thought to have an effect on the integrating mechanism of the sympathetic nervous system. This view was also supported by the experiments with neuromuscular preparation of lobster (Panulirus japonicus). It is concluded from these results, that the change of gastrointestinal motility induced by intravenous injection of Flavoxate hydrochloride (10 mg/kg) is influenced both by its effect on the gastrointestinal smooth muscle itself and by its effect via the autonomic nervous system.
Animals↗
[Effect of reduced gastrointestinal motility on the regulation of gastrointestinal flora and the pathogenesis of coli enterotoxinemia in market swine].
Opium tincture and Spasmentral were applied to piglets early after weaning and reduced their gastro-intestinal motility, which, however, caused only very minor changes in quantitative germ flora composition in those first days. Short-time suppression of gastro-intestinal motility obviously does not result in detrimental consequences to the organism as a whole, since there seem to be several factors which are involved in the control and regulation of the intestinal germ flora. Impairment of gastro-intestinal motility appeared to be of no importance to the pathogenesis of coli-enterotoxaemia, as it was not followed by higher incidence of the disease.
Animals↗
A study of the effect of vinca alkaloid 'vinblastine' on gastrointestinal motility in rats.
Vinblastine an alkaloid of the periwinkleplant (Vinca), produced marked alterations in the motility of gastrointestinal tract in rats. The alkaloid reduced the rate of gastric emptying and slowed the transit of test substance through the small intestine. The effect of the drug on gastric emptying appeared to be dose-dependent. The latency of drug action on gut motility was found to be 5--10 min, when injected through the jugular vein.
Animals↗
Effects of macrolide antibiotics on gastrointestinal motility in fasting and digestive states.
The effect of macrolide antibiotics on gastrointestinal motility was studied in unanaesthetized dogs by using strain-gauge transducers. Midecamycin acetate, leucomycin, josamycin and acetylspiramycin, which are 16-membered macrolides, did not affect the gastrointestinal motility and no symptoms of gastrointestinal disorder were observed. On the other hand, erythromycin, roxithromycin, clarithromycin and oleandomycin, which are 14-membered macrolides, caused giant contraction and disorder symptoms. Moreover, it was found that the glycosidic linkages of the lactone ring were necessary for a structure to exert strong contractile activity.
Animals↗
[Significance of in-vitro studies ofr the evaluation of gastrointestinal motility].
To study the function of the smooth muscles taken from the gastrointestinal tract the simple organ bath or various superfusion techniques can be used. With the aid of these methods it is possible to measure contractile and electrical phenomena of the isolated muscles. In addition the reactivity to various stimuli can be tested. Such in-vitro-systems elucidate principal questions of physiology, pathophysiology, and pharmacology. However, there is no direct clinical significance of in-vitro-investigations of gastrointestinal motility up til now. The clinical benefit of such investigations can be seen in the better understanding of the pathophysiology and in the discovery of new drugs in the field of gastrointestinal motility.
Digestive System Physiological Phenomena↗