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At least 973 records · Page 54Linked to original sources
PubMed1999

Effects of intraabdominally insufflated carbon dioxide and elevated intraabdominal pressure on postoperative gastrointestinal transit: an experimental study in mice.

BACKGROUND/PURPOSE: Postoperative ileus after abdominal operations is thought to be related to the degree of surgical trauma, and it has been shown that the simple act of opening the peritoneum can decrease gastrointestinal motility. Accordingly, some investigators have shown a reduction in the duration of postoperative ileus after laparoscopic procedures. It is not clear, however, if this reduction is secondary to less manipulation of the viscera or to the lack of an abdominal incision. The aim of this study was to determine the effect of intraabdominal insufflation with CO2 on postoperative gastrointestinal transit. METHODS: Twenty-eight male mice weighing between 25 and 30 g were divided randomly into 4 groups: Control (unoperated), Incision (conventional laparotomy), Cecal (laparotomy plus cecal manipulation), and Insufflation (abdominal insufflation with CO2). Postoperative gastrointestinal motility was assessed by weighing total fecal output over the first 15 postoperative hours. RESULTS: Fecal pellet output over 15 hours in the untreated control group was 1.20 +/- 0.12 g. In mice subjected to peritoneal incision alone, fecal pellet output was significantly decreased to 0.82 +/- 0.11 g (P < .05). However, in mice subjected to abdominal insufflation with CO2, fecal pellet output was not significantly different from untreated controls (1.2 +/- 0.05 g; not significant). Fecal pellet output was markedly reduced by incision combined with cecal manipulation (0.24 +/- 0.02 g, P < .01). CONCLUSIONS: The current study findings show that abdominal insufflation, in a procedure similar to that used during laparoscopic surgery, had no measurable effect on gastrointestinal transit in awake mice. This suggests that the lack of an abdominal incision can contribute to a reduced postoperative ileus after abdominal surgery.

Abdomen↗
PubMed2006

Intestinal motility disturbances in intensive care patients pathogenesis and clinical impact.

BACKGROUND: Gastrointestinal motility disturbances in critically ill patients are frequent in the ICU setting, causing considerable discomfort and are associated with increased rates of morbidity and mortality. This review focuses on the pathophysiological basis of intestinal motility, the major patterns of pathological motility alterations, the impact on patient outcome, and current therapeutic options. DISCUSSION: Intestinal motility is controlled by the enteric nervous system, modulated by hormones and extrinsic afferent and efferent neurons. Pathological motility disturbances can affect the stomach, small bowel, and colon separately or in combination. Changes in esophageal motor activity contribute to the aspiration of gastric juice, whereas early enteral feeding most frequently fails due to gastric intolerance. Disturbances in digestive and interdigestive motility patterns and the inability to switch motor activity from the interdigestive to the digestive pattern also contribute to feeding disability and thus to increased morbidity and mortality as well. CONCLUSIONS: The therapeutic options for motility disturbances in critically ill patients include the adjustment of electrolyte imbalances, tailored fluid management, early enteral feeding, appropriate management of catecholamines and drugs used for analgosedation, and prokinetic drugs. Unfortunately, the therapeutic options for treating motility disturbances in ICU patients are still limited. This situation requires careful assessment of ICU patients with respect to gut motility disturbances and their pathophysiological mechanisms and an individually tailored treatment to prevent further aggravation of existing motility disturbances.

Critical Care↗
PubMed1983

Effect of yohimbine on xylazine-induced prolongation of gastrointestinal transit in dogs.

The effect of xylazine on the transit of barium sulfate through the stomach and duodenum was evaluated in 4 dogs. Base-line transit time was determined while the dogs were nonsedated and undisturbed; the mean time for barium sulfate to move from the stomach to the duodenojejunal junction was 4.8 +/- 1.2 minutes. An IV injection of xylazine (1 mg/kg) prolonged the mean transit time to 157 +/- 37.8 minutes. During the xylazine-induced prolongation of gastrointestinal transit, there were no vigorous contractions for at least 90 minutes. Yohimbine, an alpha 2-adrenergic-blocking agent, given IV at a dosage of 0.1 mg/kg, did not affect gastrointestinal motility. It did, however, prevent both the gastrointestinal and sedative effects of xylazine. Atropine methylnitrate given IV at a dosage of 1 mg/kg prolonged the transit time to 13.8 +/- 2.4 minutes. After atropine methylnitrate injection, the gastrointestinal tract was more flaccid than with xylazine administration. The prolongation of transit induced by atropine methylnitrate was not prevented by yohimbine. It was concluded that gastrointestinal radiographic findings in animals under the influence of xylazine should be interpreted cautiously.

Animals↗
PubMed1998

Familial megacecum and colon in the rat: a new model of gastrointestinal neuromuscular dysfunction.

Gastrointestinal motility disorders are of considerable clinical importance in humans and animals. Abnormalities of smooth muscle and the enteric nervous system have been described. We have identified and characterized a new mutant stock of rats that develops severe megacecum and colon with pseudo-obstruction, Familial Megacecum and Colon (FMC). The inheritance pattern of FMC was characterized by selective breeding. Gastrointestinal motility was evaluated radiographically. Complete pathologic evaluations, including ultrastructural examination and staining of colonic segments for acetylcholinesterase, peripherin, vasoactive intestinal peptide, substance P, nitric oxide synthase, and somatostatin, were performed. Spontaneous contractility and contractile force in isolated colonic muscle strips were examined. Familial megacecum and colon is inherited as an autosomal recessive trait. The markedly dilated cecum and proximal portion of the colon are followed by a short, funnel-shaped segment and distal portion of the colon with normal or slightly reduced lumen. Although clinical features and gross anatomic changes of the colon resemble those of Hirschsprung's disease in humans and animals, aganglionosis is not a feature of FMC. An increase in somatostatin staining was observed in dilated regions of bowel. The spontaneous contractile frequency and contractile force were diminished in the affected colon. Familial megacecum and colon is a new mutant, distinct from previously described hereditary and targeted mutant rodent models that develop megacecum and colon as a result of distal colonic dysfunction. The functional or morphologic defect(s) that result in colonic dysfunction in rats with FMC was not determined. The disease may result from an absence or overexpression of a single or group of neurotransmitters or their respective neurons, receptor abnormalities, or defects in the intestinal pacemaker system.

Animals↗
PubMed1996

[Constipation after tilidine/naloxone and tramadol in comparison to codeine. A dose response study in human volunteers].

Tramadol, a mixed mu-opioid agonist and a monoamine-reuptake blocking analgesic, has been supposed to have little effect on propulsive gastrointestinal motility. However, this has not been specifically studied in man. Following institutional approval, 18 human volunteers were given 50 mg of tramadol, tilidine/naloxone, and codeine, respectively, in a double-blind randomised cross-over design. Additionally, 12 further volunteers were given 100 mg of each opioid in a double-blind, randomised fashion, followed by measurement of gastrocoecal transit time. Gastrointestinal transit time was measured using the lactulose H(2)-breath test. A threefold increase in end-expiratory hydrogen when compared to the control value was considered the end point of gastrocoecal transit. At the low dose (50 mg) the three opioids did not differ significantly with regard to their effect on gastrointestinal motility. Gastrocoecal transit time was 90.8 (+/- 10.1 SEM) min for tramadol, 100.6 (+/- 9.8 SEM) min for tilidine/naloxone, and 104.2 (+/- 8.7 SEM) min for codeine. Doubling the dose of each opioid resulted in an increase in mean gastrocoecal transit, namely 97.8 (+/- 11.2 SEM) min for tramadol, 129.2 (+/- 12.2 SEM) min for tilidine/naloxone and 135.9 (+/- 9.2 SEM) min for codeine. The increase in gastrocoecal transit time was significant (P < 0.01) for high doses of tilidine/naloxone and codeine in contrast to the effect of the low doses. This lesser constipation effect may be due to the reduced affinity of tramadol to the mu-opioid receptor. Sedation was significantly higher for codeine after 50 mg (P < 0.05) and 100 mg (P < 0.005) than for tilidine/naloxone and tramadol. Vertigo was significantly higher after 50 mg (P < 0.05) and 100 mg (P < 0.005) of tilidine/naloxone and codeine than after tramadol. Perspiration was significantly higher after tramadol 100 mg (P < 0.005) than after tilidine/naloxone and codeine. Sedation is considered a typical symptom of analgesics interacting with centrally located opioid receptor sites. The higher incidence of perspiration after tramadol suggests that monominergic pathways may be involved in thermoregulation. In conclusion, the opioids tilidine/naloxone and codeine at the doses used significantly prolong gastrointestinal transit time in the high-dose range. Since tramadol does not induce a dose-related increase in gastrocoecal transit time, it may be a useful analgesic in patients who are prone to developing constipation during high-dose opioid therapy.

Clinical Trial↗
PubMed1997

[Quantitative evaluation of diabetic gastrointestinal paresis by measuring transit time of the stomach and the digestive canal].

Our subjects comprised eighty six diabetes mellitus (DM) patients without severe complication. To evaluate gastrointestinal motility quantitatively, we measured gastric emptying time by acetaminophen (APAP) method using serum APAP value and oro-cecal transit time (OCTT) by lactulose hydrogen breath test in the subjects and normal controls (NC). Comparing DM patients and NC, mean APAP value was lower and mean OCTT was prolonged in the former. Analysing DM patients' background, patients with peripheral neuropathy had prolonged OCTT than patients without neuropathy did. Comparing patients with higher HbA1c levels and patients with normal HbA1c levels, mean APAP value, which was closer to normal levels, was higher in the former. Analysing symptoms, some of them were apparently related to abnormal gastrointestinal motility. From these results, it was concluded that measuring both gastric emptying and OCTT was a useful method to evaluate slight abnormal motility in DM patients.

Diabetes Mellitus↗
PubMed1994

Magnetic markers as a noninvasive tool to monitor gastrointestinal transit.

A novel method to monitor gastrointestinal transit of solid oral dosage forms or nutrients is presented, providing a simultaneous recording of gastrointestinal motility of the traversed section. Based on the measurement of the magnetic field of an ingested magnetized marker, its location is found by fitting a magnetic dipole field to the measured data.

Gastrointestinal Motility↗
PubMed2001

The effect of different dosages of guar gum on gastric emptying and small intestinal transit of a consumed semisolid meal.

BACKGROUND: There is no consensus about the effect of guar gum supplementation on gastrointestinal transit. It has been suggested that guar gum slows gastric emptying and intestinal transit, thus inducing an increased feeling of satiety. OBJECTIVE: To investigate whether addition of guar gum to a semisolid meal affects gastrointestinal transit. DESIGN: Eight male subjects were randomly studied four times. They consumed a standard semisolid test meal containing either 0 g, 2.5 g, 3.5 g, or 4.5 g of guar gum. The test meals contained 1 mCi 99mTc-hepatate for scintigraphy and 5 g lactulose for the H2-breath test. Scintigraphic scanning was performed for at least two hours, and gastric half-emptying time (T1/2) was calculated. Breath samples were collected at 15 minute intervals and analyzed for H2-enrichment. The orocecal transit time (OCTT) was then determined. A parameter of intestinal transit (PIT) was obtained by subtracting the T1/2 from the OCTT. RESULTS: There were no significant differences (in minutes) between the different tests in both T1/2 (0 g, t = 88.2 +/- 11, 2.5 g, t = 83.3 +/- 11.9, 3.5 g, t = 83.3 +/- 13.6, 4.5 g, t = 72.4 +/- 7.2, p = 0.86) and PIT (0 g, t = 149.9 +/- 26.6, 2.5 g, t = 145.5 +/- 25.6, t = 3.5 g, t = 175.3 +/- 17.6, t = 4.5 g, t = 152.6 +/- 22.4, p = 0.52). CONCLUSION: Addition of guar gum to a semisolid meal up to a dosage of 4.5 g does not affect gastrointestinal transit. Other mechanisms than gastrointestinal motility are involved in a possible satiating effect of guar gum supplementation.

Adult↗
PubMedDate not supplied

[Breath tests in the diagnosis of gastrointestinal diseases].

Determination of carbon or hydrogen markers in breath has allowed closer investigation of the pathogenic mechanisms of several gastrointestinal diseases. Thus, the 13C-urea breath test is a nonaggressive, simple and safe test with excellent accuracy both in the initial diagnosis of Helicobacter pylori infection and in confirmation of its eradication following treatment. Moreover, because of the simplicity, reproducibility and safety of these types of procedure, they have tended to substitute more uncomfortable and expensive techniques that were traditionally used in gastroenterology. Several breath tests have been developed that allow reliable evaluation of liver or exocrine pancreatic function, gastrointestinal motility, as related to gastric emptying or orocecal transit time, and a diagnostic approach to clinical problems that could be due to bacterial overgrowth or malabsorption of various sugars.

Breath Tests↗
PubMed1990

Delayed stomach to caecum transit time in the diabetic rat. Possible role of hyperglucagonaemia.

Disturbances of gastrointestinal motility are a common feature of diabetes mellitus and are usually ascribed to autonomic neuropathy. In order to assess the role of other factors on changes in motility in diabetes we have studied the stomach to caecum transit time (SCTT) during the progression of streptozotocin induced diabetes in the rat. Rats were used one, two, four, and eight weeks after a single injection of streptozotocin and age matched animals were used as controls. In further experiments non-diabetic rats received a bolus injection of pancreatic glucagon (50 or 75 micrograms intraperitoneally) or its diluent. SCTT was estimated using the non-invasive hydrogen excretion method. SCTT was unaffected by the age of the animal (mean (SEM) value: 101 (5) min), but was significantly delayed at one week (139 (11) min, p less than 0.01), two weeks (163 (16) min, p less than 0.01), four weeks (148 (9) min, p less than 0.01), and eight weeks (171 (13) min, p less than 0.01) after streptozotocin. SCTT was also slower during hyperglucagonaemia (control 96 (6) min; glucagon treated 50 micrograms: 120 (7) min, p less than 0.05 and 75 micrograms: 127 (8), p less than 0.05). Since autonomic neuropathy is not a recognised feature of the initial stages of diabetes hyperglucagonaemia may be responsible, at least in part, for diabetes induced changes in gastrointestinal motility.

Animals↗
PubMed2003

Alosetron and irritable bowel syndrome.

Alosetron (Lotronex, GlaxoSmithKline) is a potent and selective 5-HT(3)-receptor antagonist approved by the FDA for the treatment of women with diarrhoea-predominant irritable bowel syndrome (IBS) in whom conventional therapy has failed. Studies involving healthy volunteers and IBS patients have demonstrated a beneficial effect of treatment with alosetron on global IBS symptoms, abdominal pain and discomfort, altered bowel function as well as improvement of quality of life (QOL). Data from animals studies suggest the involvement of 5-HT(3) receptors on intrinsic primary afferent neurons in the mediation of the effect of alosetron on gastrointestinal motility and secretion. While definitive proof of a visceroanalgesic action is not available, an additional central mechanism of action is suggested by findings obtained in animal models, as well as from human brain imaging studies. Alosetron shows a greater effectiveness in women, and the role of genetic factors underlying inter-individual differences in the response to alosetron is currently under investigation. The most frequent adverse event associated with the use of alosetron is constipation and in some rare cases, the development of colonic mucosal ischaemia. In the following review, the most recent reported effects of alosetron on gastrointestinal motility, visceral sensitivity and anxiety, both in terms of preclinical and clinical data will be discussed. The impact of alosetron on QOL in IBS patients and the safety of treatment with alosetron, will also be covered.

Carbolines↗
PubMed1994

Drugs affecting serotonin receptors.

A greater understanding of the various serotonin receptor subtypes has led to a clearer appreciation of the role of serotonin in gastrointestinal motility, sensation and secretion. Serotonin is definitely involved in the aetiopathogenesis of cisplatin-induced emesis and carcinoid diarrhoea. The application of serotonergic drugs in clinical therapeutics for gut disturbances is presently dominated by the use of 5-HT3 antagonists for acute chemotherapy-induced nausea and vomiting, and the use of substituted benzamides which are 5-HT4 agonists stimulating gut motor function through 5-HT4 neuronal receptors. The best-studied 5-HT4 agonist is cisapride, which has been shown to stimulate motility at several levels of the gut. Cisapride is approved for healing and maintenance treatment of reflux oesophagitis and is used in several countries for the alleviation of symptoms consistent with regional stasis, from dyspepsia to constipation. Carcinoid diarrhoea is a prototypic disease associated with deranged serotonin metabolism, and a rationale for using 5-HT3 or 5-HT4 antagonists is based on the recent appreciation of the important role of impaired gut motor function in carcinoid diarrhoea. In the future, greater understanding of the serotonin receptor subtypes and their role in gut disorders may lead to novel approaches to alleviate increased visceral perception of functional gastrointestinal disorders, to correct changes in colonic capacitance, or to alter gastrointestinal motility that contributes to diarrhoea or constipation. However, at the present time, it must be stressed that these uses are still at an experimental stage and that careful validation and proper controlled studies are still required.

Animals↗
PubMed2003

Ion channels in gastrointestinal smooth muscle and interstitial cells of Cajal.

A requirement for normal gastrointestinal motility is the tight regulation of ion channels expressed in interstitial cells of Cajal and smooth muscle. Interstitial cells of Cajal generate the slow wave and amplify neuronal signals; smooth muscle functions as the final effector organ. Recent advances in our understanding of the expression and mechano-regulation of these different subtypes of ion channels have allowed the development of hypotheses on how ion channels transduce a variety of inputs into electrical signals that directly or indirectly regulate gastrointestinal motor activity.

Calcium Channels↗
PubMed1998

Effect of estradiol on rat ileum.

1. Sex hormones may influence gastrointestinal motility and thus may be responsible for symptoms that are common during pregnancy or hormone replacement therapy. The purpose of this study was to evaluate the effect of estradiol on the gut. 2. Segments of rat ileum (n=9) were suspended in an organ bath and exposed to increasing concentrations of carbachol, in the presence or absence of 17beta-estradiol. 17beta-estradiol markedly reduced the force developed by the ileum in response to carbachol. 3. These results suggest that estradiol reduces gastrointestinal motility.

Animals↗
PubMed1989

Role of cholecystokinin in regulation of gastrointestinal motor functions.

By means of loxiglumide, a potent and highly specific antagonist for cholecystokinin (CCK), the effects of blocking CCK receptors on gastrointestinal motility were investigated in a placebo-controlled study in healthy young men (aged 21-39, mean 24 years). Gallbladder contraction stimulated by ingestion of a liquid test meal was completely abolished by oral administration of loxiglumide 30 min before the test meal. Gastric emptying of radio-opaque markers ingested with the test meal was significantly accelerated by loxiglumide (area under the curve [markers x h] 33.3 [SEM 3.8] vs 17.9 [2.7] after placebo). No effect of loxiglumide was found on small-bowel transit time, but 7 days' treatment with oral loxiglumide (800 mg three times daily) significantly shortened colonic transit time (29.4 [4.1] h after placebo, 15.0 [3.4] h after loxiglumide). It is concluded that CCK is an important mediator of meal-induced gallbladder contraction and is involved in the regulation of gastrointestinal motility in man.

4-Aminobenzoic Acid↗
PubMed2005

Effect of sodium fluoride on gastric emptying and intestinal transit in mice.

Fluoride, a well-recognised harmful substance, is easily absorbed by the gastrointestinal mucosa. It is therefore conceivable that any alteration of the gastrointestinal motility can affect the rate of absorption of fluoride and leads to aggravation of its toxic effects. The effects of fluoride on gastric emptying and intestinal transit were studied in the mouse using a carboxymethyl cellulose (CMC) solution as a non-nutrient meal. The participation of the cholinergic and nitrergic systems in these effects was also evaluated. Oral gavage of 5 mM NaF had no significant effect on gastric emptying and intestinal transit of the CMC meal, whereas a decrease of gastric emptying (-33%, P<0.05) and an increase in intestinal transit (+20.7%, P<0.05) were observed with 20 mM NaF. Atropine injection induced a significant decrease of gastric emptying. Combined treatment of atropine with 20 mM NaF brought about a further, but not significant decrease in gastric emptying. N-G-nitro-L-arginine-methyl ester (L-NAME) treatment with or without oral administration of NaF decreased gastric emptying. Atropine treatment significantly depressed intestinal transit from 56.5% to 37.7% in the absence of NaF and from 70.1% to 42.8% in its presence. In contrast, L-NAME administration either alone or with fluoride increased intestinal transit (P<0.05). The present results suggest that fluoride alter gastrointestinal motility, an effect that may partly involve the cholinergic pathway.

Administration, Oral↗
PubMed1982

Effect of metoclopramide in guinea-pig ileum longitudinal muscle: evidence against dopamine-mediation.

The investigation examines the hypothesis that metoclopramide-induced potentiation of gastrointestinal motility is mediated through dopamine receptors. In vitro studies on the longitudinal muscle of the guinea-pig ileum were performed. Metoclopramide, in concentrations comparable with those seen in plasma after therapeutic doses in man, selectively potentiated the cholinergic response Dopamine (1-100 microM) inhibited cholinergic transmission by inhibiting neuronal acetylcholine release. The inhibitory action of dopamine was antagonised by phentolamine, and alpha-adrenoceptor antagonist, but not by the dopamine receptor antagonists metoclopramide or primozide. Bromocriptine inhibited cholinergic responses by a postsynaptic mechanism which was not antagonised by metoclopramide, primozide, or phentolamine. The results are consistent with the view that metoclopramide-induced potentiation of gastrointestinal motility does not involve local dopamine receptors.

Animals↗
PubMedDate not supplied

Melatonin and the gastrointestinal tract.

Melatonin has been detected in the digestive tract of several species and appears to be synthesized by the enterochromaffin cells of the gut. Although a diurnal rhythm of melatonin release has been observed in gastrointestinal tissues of birds, in other species it seems to depend on the presence of nutritional elements. Melatonin binding sites have been identified in the digestive tract of several species and it has been suggested that melatonin could act as a protecting agent of the gastrointestinal mucosa. Moreover, the potential role of melatonin as a local regulator of gastrointestinal motility has been investigated. It seems that at least some effects of melatonin on gut activity depend on an antagonistic relationship between serotonin and melatonin. The effects of melatonin on segmental gut transit both in the fasting and in the fed state, as well as on the electromyographic pattern of the small intestine in rats, are described.

Animals↗