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At least 37 records · Page 2Linked to original sources
PubMed1998

Effect of octreotide on gastrointestinal motility in children with functional gastrointestinal symptoms.

BACKGROUND: The somatostatin analogue octreotide has been proposed as a possible therapeutic agent in patients with abnormal gastrointestinal motility. This study was conducted to study the effects of 0.5 microg/kg and 1.0 microg/kg subcutaneous octreotide on antroduodenal motility in children with chronic gastrointestinal disorders. METHODS: Twenty-three children were studied, eight with intestinal pseudo-obstruction, six with nonulcer dyspepsia, six with gastroesophageal reflux disease, and three with intractable constipation. After recording fasting motility for more than 4 hours, the children were randomized to receive 0.5 microg/kg or 1 microg/kg of subcutaneous octreotide. Motility was recorded for another hour after feeding in 12 children. RESULTS: Phase III of the motor migrating complex was present in 13 of 23 children before and in 21 after octreotide (p < 0.02). All phase III episodes after administration of octreotide except one originated in the small intestine. Phase IIIs after octreotide were longer and were propagated faster than the spontaneous phase IIIs. There were no antral contractions during fasting after octreotide. There was a significant decrease in phase II intestinal motor activity in the hour after administration of octreotide (p < 0.001). There was no difference in effect between the two doses. After feeding, antral contractions were present in all children, and intestinal phase IIIs were not abolished. CONCLUSIONS: In children with chronic bowel disorders, subcutaneous octreotide induced phase IIIs that differed from spontaneous phase IIIs and were not inhibited by meals. Octreotide decreased antral motility during fasting and inhibited intestinal phase II. Feeding abolished the inhibitory effect of octreotide on antral motility.

Adolescent↗
PubMed1992

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↗
PubMed1984

[Control of gastrointestinal motility and secretion by gastrointestinal peptides].

Cyclic pattern of interdigestive motility and of plasma levels of motilin, somatostatin and pancreatic peptide (PP) show close relationship. During interdigestive state gastric and lower esophageal motility seems to be mediated by pulsatile release of motilin, whereas the motor activity of duodenum seems to be controlled by somatostatin. Disturbed interdigestive motility could be demonstrated in gastrointestinal diseases like bacterial overgrowth, sclerodermia, post-vagotomy diarrhea and reflux esophagitis.

Diarrhea↗
PubMed1994

Effects of hyperglycemia on interdigestive gastrointestinal motility in humans.

BACKGROUND: Gastrointestinal motility disorders are common in patients with diabetes mellitus. Recent studies indicate that hyperglycemia can affect gastric emptying and gastric motility in healthy subjects and diabetics. METHODS: The effect of acute hyperglycemia on gastrointestinal motility was studied with a manometric technique in healthy subjects. Seven individuals, four men and three women, 23-34 years old, were studied on 2 different days. On 1 of the days a 5-h registration was performed after an overnight fast. On another day and after an initial basal period, acute steady-state hyperglycemia was induced by intravenous glucose infusion for 90 min. Motility variables were evaluated in four segments: in the gastric antrum, the proximal duodenum, the distal duodenum, and the proximal jejunum. RESULTS: Fasting migrating motor complex rhythm including migration of phase III prevailed during hyperglycemia. Compared with euglycemia, the motility index in phase II was lower during hyperglycemia in all segments studied. In the antrum the difference was 62% (p < 0.01); in the proximal duodenum, 37% (p < 0.01); in the distal duodenum, 44% (p < 0.05); and in the jejunum, 58% (p < 0.01). During hyperglycemia the prevalence of propagated contractions in phase II was significantly lower than during euglycemia both in the antrum and the proximal duodenum. In the last part of phase III in proximal duodenum most individual contractions were propagated in orad direction compared with early phase III, and this difference persisted during hyperglycemia. The number of long clusters was significantly increased during hyperglycemia as compared with euglycemia: 2.0 +/- 0.6 per hour versus 0.4 +/- 0.14 (p < 0.01). In late phase II plasma levels of motilin and pancreatic polypeptide were significantly decreased during hyperglycemia. CONCLUSION: Hyperglycemia not only reduces the motility in the stomach but also inhibits motility in both the duodenum and the jejunum. The results show that acute hyperglycemia has an important impact on small-intestinal motility.

Adult↗
PubMed1992

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↗
PubMed1994

Comparison of the effects of midecamycin acetate and azithromycin on gastrointestinal motility in man.

The gastrointestinal motor effects of the macrolide antibiotic, azithromycin, 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. Eleven healthy volunteers participated in the single blind, placebo-controlled study of both interdigestive and postprandial gastrointestinal motility. Azithromycin was administered by mouth in a single 500 mg dose or in two daily doses of 250 mg; 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. Peroral treatment with azithromycin resulted in a statistically significant increase in the postprandial antral motility index as compared to placebo. This increase was observed in the distal antrum as well as in the proximal antrum. In addition, the gastric contractions were found to originate higher up in the stomach after azithromycin as compared to placebo or midecamycin acetate.

Adult↗
PubMed1995

Drugs coordinating and restoring gastrointestinal motility and their effect on selected hypodynamic gastrointestinal disorders in horses and cattle.

Hypodynamic gastrointestinal disorders in horses and cattle that are thought to benefit from treatment with drugs restoring and coordinating gastrointestinal motility include postoperative ileus and large colon impaction in the horse and displacement of the abomasum and dilatation of the cecum in cattle. Important physiologic, pathophysiologic and pharmacologic mechanisms involved in the intrinsic control of gastrointestinal motility include cholinergic, adrenergic, dopaminergic, serotoninergic, and opioid-mediated pathways. Preliminary results suggest that cisapride, acting on 5-Hydroxytryptamine receptors, might be useful for treatment of idiopathic postoperative ileus and the alpha 2-adrenoceptor blocking agent yohimbine for endotoxic postoperative ileus. Naloxone, an opioid antagonist, and neostigmine, an acetylcholinesterase inhibitor, are thought to restore motility of the large colon in cases of large colon impaction in the horse. Bethanechol and neostigmine significantly increase myoelectric activity of the cecum and proximal loop of the ascending colon in healthy cows. Investigations of the effects of prokinetic drugs on displacement of the abomasum of cattle do not allow any conclusions because no results derived from controlled experimental disease models are available.

Adrenergic Antagonists↗
PubMed2002

Aging and neural control of the GI tract: IV. Clinical and physiological aspects of gastrointestinal motility and aging.

The gastrointestinal motility changes that occur as a function of age are reviewed herein. Careful attention must be given in any review of aging phenomena to exclude, or at least be cognizant of, the many comorbid conditions that can alter physiological functioning in older adults. The dramatic increase in life expectancy over the past 10-15 years demands that clinicians be aware of the various physiological and clinically relevant changes that occur with age. Gastrointestinal motility changes associated with age are relatively subtle, and in many instances only conflicting data exist. As the older adult population increases, and as the control of disease is improved, much more work needs to be done to understand the true effects of aging on gastrointestinal functioning.

Aged↗
PubMed2000

The impact of chronic hepatitis B viral infection on gastrointestinal motility.

OBJECTIVES: Disturbed gastrointestinal (GI) motility probably exists in alcoholic cirrhotic patients; however, the influence of chronic hepatitis B virus (HBV) infection on GI motility remains unknown. The purpose of this prospective study was to determine the impact of chronic HBV infection on human GI transit, and to explore the possible patient factors modulating GI motility. METHODS: We used a non-invasive hydrogen breath test measuring the oro-caecal transit time (OCTT) to assess the GI motility in 45 asymptomatic HBV carriers, 26 patients with chronic hepatitis B, 23 patients with HBV-related liver cirrhosis, and 45 age- and sex-matched healthy volunteers. Their clinical symptoms and various blood parameters, such as platelet count, prothrombin time, etc. were recorded. Plasma substance P, nitrate/nitrite and endothelin-1 levels were also measured. RESULTS: The OCTTs in controls, HBV carriers, chronic hepatitis B and liver cirrhosis patients were (mean +/- SEM) 78.4 +/- 5.8, 80.9 +/- 4.2, 93.9 +/- 8.8 and 106.5 +/- 12.4 min, respectively. The OCTT was delayed in patients with HBV-related liver cirrhosis compared to that of controls (P=0.039). Among the cirrhotic patients, presentation with ascites delayed OCTT (145.7 +/- 27.2 versus 91.3 +/- 11.9 min, P=0.039). Neither Child- Pugh grade, portal hypertension, various blood parameters, plasma substance P, nitrate/nitrite or endothelin-1 levels had any influence on OCTT. CONCLUSIONS: HBV infection alone does not alter GI motility, whereas the patients with liver cirrhosis may have delayed GI motility. Ascites is most likely a factor responsible for the delayed GI transit among chronic HBV-infected subjects.

Aged↗
PubMed1990

Effect of casein and beta-casomorphins on gastrointestinal motility in rats.

The effect of bovine casein and synthetic beta-casomorphins on the motility of rat gastrointestinal tract was studied by noninvasive techniques using the nonabsorbable marker 141Ce. Casein suspensions (CAS) or whey protein suspensions (WPS) were labeled with 141Ce and fed by gastric tube. Gastric emptying rate (GER) as well as gastrointestinal transit time (GITT) of the tracer were significantly longer with feeding CAS compared to WPS. The differences between the CAS and the WPS groups were partly (GER) or completely (GITT) abolished by pretreating the animals with the specific opiate-receptor antagonist naloxone. It is assumed that opioid peptides released from casein during digestion slowed gastrointestinal motility by direct interaction with gut opiate receptors. To prove whether beta-casomorphins, when given by gastric tube, can affect motility, different synthetic beta-casomorphins in doses between 1 and 10 mg were added to the WPS. The beta-casomorphin-4 (Tyr-Pro-Phe-Pro-NH2) showed no effect on GITT. The D-Ala substituted D-Ala-beta-casomorphin-4 (Tyr-D-Ala-Phe-Pro-NH2) and D-Ala-beta-casomorphin-5 (Tyr-D-Ala-Phe-D-Ala-Tyr-NH2), which are more resistant to proteolytic attack and have higher opioid potency than beta-casomorphin-4, slowed GITT in a dose-dependent manner.

Amino Acid Sequence↗
PubMed1996

Effects of parenteral nutrients on gastrointestinal motility and secretion.

BACKGROUND: The stimulation of gastrointestinal motility and secretion during nutrient digestion is generally divided into a cephalic, gastric and intestinal phase. Little is known about the effects of macronutrients on gastrointestinal function during the postabsorptive or circulatory phase of digestion. METHODS: Review of studies investigating the effects of circulating macro-nutrients such as fat, amino acids and glucose on gastrointestinal motility and secretion. RESULTS: Intravenous infusion of fat emulsions delays gastric emptying and interrupts the interdigestive intestinal motor pattern. Intravenous amino acids, administered in high doses, stimulate gastric acid secretion, pancreatic secretion, gallbladder contraction, and intestinal motility. Patients receiving total parental nutrition (TPN) have inert gallbladders and are at risk of developing gallbladder sludge and stones. Administering a proportion of the daily amino acid requirement by rapid intravenous infusion may prove useful in the prevention of sludge and stone formation during TPN by promoting gallbladder contraction. Intravenous infusion of glucose, already at physiological postprandial plasma levels, inhibits gastrointestinal motility and secretion. The inhibitory effect of glucose is dose-dependent, that is, more pronounced at higher plasma glucose levels. Recent studies have indicated that in patients with diabetes mellitus alterations in gastrointestinal function are related to the degree of hyperglycaemia. CONCLUSIONS: Nutrients during the circulatory phase of digestion influence gastrointestinal motility and secretion. Knowledge of these effects is relevant for conditions with increased plasma levels of macro-nutrients such as in patients with diabetes mellitus or during total parenteral nutrition.

Gastrointestinal Motility↗
PubMed1989

Rational pharmacotherapy of gastrointestinal motility disorders.

Nervous control of gastrointestinal motility is extremely complex, is regulated by the enteric system, the "brain of the gut", and modulated by extrinsic nerves. This system with its multiplicity of transmitters and receptors does not always allow a clear interpretation of experimental data, especially with compounds lacking specificity. In this review the complex situation is described particularly in relation to receptor populations (cholinergic, adrenergic, dopamine, histamine, 5-hydroxytryptamine, opioid, gamma-aminobutyric acid (GABA), prostanoid and dihydropyridine receptors), therapeutic aspects of drugs and their usefulness in children. Newer principles with known drugs and promising new compounds with a more appropriate kinetic or fewer side-effects, deriving from distinct pharmacological groups, as candidates for the treatment of gastrointestinal disorders are considered e.g. anticholinergics (prifinium or actilonium bromide), adrenergic alpha 2-agonists (clonidine, lidamidine) for diarrhoea in diabetic neuropathy, adrenergic beta-blockers for shortening postoperative ileus (propranolol), dopamine receptor antagonists (metoclopramide, domperidone, alizapride) and another prokinetic substance (cisapride) which may be useful for a number of applications as gastro-oesophageal reflux, gastro-paresis, intestinal pseudo-obstruction, cystic fibrosis and constipation, morphine derivatives (e.g. loperamide) for intractable diarrhoea and calcium antagonists (e.g. nifedipine) for achalasia. Increasing experience in digestive tract pharmacology and reliable clinical studies will furthermore be the basis for a more specific and better tolerated therapy of gastrointestinal motility disorders in adults and children.

Child↗
PubMed2001

[The effect of calponin and caldesmon in regulation of the gastrointestinal motility during pathophysiological adaptation].

OBJECTIVE: To investigate the expression of calponin (CaP) and caldesmon (CaD) in the gastrointestinal tract and their effect in regulating gastrointestinal motility during physiological and pathological adaptation. METHODS: Models of chronic gastrointestinal motility hyperfunction in mice were induced by intragastric administration of senna extraction and models of chronic gastrointestinal motility hypofunction in rats were established with carbon tetrachloride induced cirrhosis, CaP and CaD were detected in the gastrointestinal tract of different model groups using SDS-PAGE and Western blot. The color development of Western blots was scanned using densitometric scanning. The relative contents of gastrointestinal CaP and CaD were compared with control animals with different state of gastrointestinal motility. RESULTS: Animal models of abnormal gastrointestinal motility were established in mice and rats. Densitometric quantification of CaP and CaD blots by CP1 and C98 mAbs showed that normal animal colon contained higher amounts of h1-CaP and CaD. In normal mice and rats, the content of CaP and CaD was successively in this order :colon > stomach > small intestine. The content was reduced in mice of chronic gastrointestinal motility hyperfunction, but the expression of CaP and CaD was promoted in rats with cirrhosis and declined to normal level after treatment with L-NAME. CONCLUSION: There is close relation between expression of CaP and CaD and state of gastrointestinal motility. CaP and CaD may inhibit gastrointestinal motility. These suggest that CaP and CaD may play a role in the regulation of gastrointestinal motility during physiological and pathological adaptation.

Animals↗
PubMed1991

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↗
PubMed1993

[Drugs and assessment of gastrointestinal motility].

Any determination of gastrointestinal motility is based on two assumptions: (1) That the patient is examined in "physiological" conditions and (2) that the values measured truly reflect the parameter the investigator wishes to examine. A large array of very different drugs shares the ability to modify the digestive motility (i.e. gastrokinetics) or to alter the content of the digestive tube in such a way that it affects the outcome of some measurements (i.e. acid suppression leads to false results in ph-metry dependent methods). Therefore, it seems advisable to ask the patient whether he is taking any drug--including non prescription medications--and check if this substance or type of substances could affect the outcome of the motility measurement envisioned. In this paper, the authors present a list of the principal drugs known to affect different motility-measurement methods. The real or apparent stimulating or inhibitory effects of drugs on four main segments of the digestive tube (esophagus, stomach, small intestines and colon) are indicated in an alphabetically ordered table. In a short review, the drugs are broadly classified according to their mechanism and site of action. Besides a number of drugs used in practice because of their action on the enteric nervous system, there is a large spectrum of compounds affecting motility, whose main therapeutic application lies outside the digestive tract, such as: psychotropic drugs, antiparkinsonian drugs, bronchodilators, antitussives, antihistamines, antimigraine drugs, antihypertensive agents, etc. This second category is more likely to escape unnoticed as a potential source of false results in the measurement of digestive motility.

Depression, Chemical↗
PubMed1986

Ontogeny of the gastrointestinal motility in young broilers.

Gastrointestinal motility of young broilers (1, 8 and 15 days old) was measured by means of 14C-polyethylene glycol-4000. Two motor patterns can be observed: GI segments anterior to ileum increased their motility proportionally to the broiler age. GI segments below ileum decreased their motility when the broiler age is increased. It is concluded that these motor patterns are due to immaturity of gastric motility, early learning of food intake regulation and/or interference between prenatal and postnatal nutrition. Proventriculus and duodenal loop showed to be transit segments, with independence of the broiler age.

Age Factors↗