Somatostatin and gastrointestinal secretion and motility.
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Gastric Juice↗
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Neural inhibition of gastrointestinal smooth muscle motility in guinea-pigs.
The neural inhibition of the gastrointestinal (GI) smooth muscle motility was studied by means of electrical transmural nerve stimulation (ETNS) in guinea-pigs. In untreated muscle strips, ETNS induced four types of response, consisting of three basic components, i.e., contraction and relaxation during ETNS, and after-contraction. Following atropinization, all the responses changed to only one type, i.e., relaxation during ETNS followed by after-contraction. The relaxation of the muscle strips induced by ETNS after atropinization was not significantly reduced under superimposing guanethidine treatment in any site of the GI tract. The maximal relaxation of the muscle strips induced by ETNS after atropine and guanethidine treatments was not uniform throughout the GI tract. The relaxation of the gastric body and colon was greater than that of the jejunum and ileum. The extent of the relaxation was significantly different even in the colon. Theophylline and phentolamine did not reduce the ETNS-induced relaxation following atropine and guanethidine treatments in the distal colon and taenia coli. The findings suggest the following: the non-adrenergic inhibitory (NAI) nerve is the main postganglionic nerve to inhibit the GI smooth muscle motility; and the role of adrenergic nerve is of little importance in respect to postganglionic inhibition. The innervation of the NAI nerve seems not to be uniform throughout the GI tract. Theophylline and phentolamine are not the specific antagonists of the NAI nerve.
Adrenergic Fibers↗
[Characterization of pacemaking currents in cultured interstitial cells of Cajal from mice small intestine].
BACKGROUND/AIMS: Gastrointestinal motility is initiated by the periodic generation of slow waves. Interstitial cells of Cajal (ICC) are pacemaker cells that generate slow waves and drive spontaneous mechanical contractions of the gastrointestinal smooth muscle. Slow waves generate the periodic activation of spontaneous inward currents (pacemaker currents). The aim of this study was to investigate the characterization of pacemaker currents of ICC. METHODS: The ICC in mice small intestine were cultured with stem cell factor for 2 days, and then we recorded pacemaker currents and slow waves using a whole-cell patch clamp technique. RESULTS: Under voltage clamp at -80 mV of holding potential, ICC generated pacemaker currents. Tetrodotoxin and nifedipine did not affect on the pacemaker currents. In addition, tetraethylammonium, 4-aminopyridine and glibenclamide did not affect on the pacemaker currents. The reduction of external Na+ concentrations inhibited pacemaker currents. Moreover, these currents were completely abolished in the external Ca2+-free condition. Gadolinium and flufenamic acid, inhibitors of non-selective cationic currents, inhibited pacemaker currents. Thapsigargin and cyclopiazoic acid, inhibitors of Ca2+-ATPase in endoplasmic reticulum, abolished pacemaker currents. Carbachol depolarized membrane potential and increased inward currents. CONCLUSIONS: These results suggest that pacemaker currents are mediated by the activation of non-selective cation channel and become a target of neurotransmitters in regulation of intestinal motility.
Animals↗
Gastrointestinal transit in thyroid disease.
Diarrhea and malabsorption are common manifestations of hyperthyroidism, whereas constipation or obstipation frequently occur in hypothyroidism. Abnormalities of gastrointestinal motility have been proposed as the primary cause of these complaints, but documentation has been conflicting and largely limited to observations of the transit time of a barium meal. We studied gastrointestinal transit time in fasting patients with thyroid dysfunction using the pulmonary excretion of H2 after the ingestion of a nonabsorbable carbohydrate, lactulose, as an indicator of the rate of transit to the colon. Mean transit time of 10 hyperthyroid patients (29 +/- 4.0 min) was significantly less than that of 42 healthy controls (72 +/- 3.7 min, p less than 0.001), and of 6 hyperthyroid patients when they became hypothyroid after treatment (80 +/- 11.0 min, p less than 0.05). Transit time decreased significantly when hypothyroid patients were given thyroid replacement (p less than 0.01). These findings support the hypothesis that abnormal gut motility may be the primary cause of the diarrhea and malabsorption of hyperthyroidism, and the constipation and obstipation commonly seen in hypothyroidism.
Adult↗
Prolonged monitoring of the upper gastrointestinal tract using echo planar magnetic resonance imaging.
Upper gastrointestinal motility and transit has been studied in five human volunteers with the ultra high speed, magnetic resonance imaging (MRI) technique MBEST (Modulus Blipped Echo-planar Single pulse Technique), a variant of echo planar imaging. Snapshot images requiring a data acquisition time of only 64-128 msec allowed visualisation of peristalsis in the antrum and duodenum in real time, without motional image degradation, as would normally be seen using conventional MRI. Gastroduodenal flow of the luminal contents was visualised using water as a contrast medium, with appropriate adjustment of the time constant (T2) weighting of the system. Rapid (0.3 Hz) imaging of gastroduodenal motility in both transverse and coronal planes was achieved by respiratory gating to the imaging frequency, allowing repetition rates of up to 20 frames per minute for 2-3 hours. Fast replay of stored images, to produce a 'movie loop', allowed identification of fasting motility patterns of the gastric antrum and proximal small intestine, with depiction of the phases of the migrating motor complex. Images of the fed patterns after the ingestion of a test meal showed good separation of solid and liquid particulate matter and mixing waves in the gastric body. The potential for quantitative measurements with this new imaging modality of the gastrointestinal tract is under development, which will allow us to measure transit and correlate this with motility data.
Adult↗
Using erythromycin. Some helpful observations.
Erythromycin is a very safe antibiotic that is effective against a wide variety of common and uncommon bacterial infections. Several formulations are available, each with a different absorption rate and dosing profile. The most common side effect of erythromycin is gastrointestinal intolerance, which appears to be related to disruption of intestinal motility. Gastrointestinal tolerance may be improved by limiting daily doses to less than 4 g; temporarily decreasing the total daily dose; using small doses of liquid suspension every 2, 3, or 4 hours; taking the medication with milk or food; and drinking water every 15 minutes two or three times after each dose. These measures may, in turn, improve compliance and efficacy in affected patients.
Drug Interactions↗
Open label study of long-term effectiveness of cisapride in patients with idiopathic gastroparesis.
Cisapride induces acetylcholine release in cells of the myenteric plexus, thus promoting gastrointestinal motility. We studied the effects of cisapride on 11 patients with idiopathic gastroparesis. All had negative gastrointestinal endoscopy, normal glucose, and took no drugs capable of influencing motility. Most (9/11) were prior metoclopramide treatment failures. Patients' symptoms were scored (0-60) for pain, satiety, bloating, nausea, vomiting, and heartburn. All underwent a solid gastric emptying study using a Technetium-99-labeled egg meal and received placebo prior to cisapride. There were 10 females and one male with a mean (+/- SE) age of 37.8 +/- 2.6 years. Disease duration was 7.9 +/- 2.8 years. The dose of cisapride was 30-60 mg/day and the duration of therapy was 12.6 +/- 2.6 months (range 2.5-25 months). The symptom score improved on cisapride from 30.9 +/- 3.6 to 14.4 +/- 2.7 (P < 0.002 signed rank test). Emptying half-time improved from 113 +/- 4 min to 94 +/- 6 min, and 46.9 +/- 2.4% food remaining at 120 min decreased to 35.5 +/- 3.6% (both P < 0.05). Emptying half-time in normals was 68 +/- 5 min with 16.9 +/- 2.9% remaining at 120 min. Nine of 11 patients gained weight, with a mean increase of 6.7 +/- 1.6 lb (range 2-12 lb). We conclude that cisapride significantly reduces gastrointestinal symptoms and promotes weight gain in patients with idiopathic gastroparesis and is associated with improvement in solid gastric emptying. The drug is useful in patients who previously failed metoclopramide.
Adult↗
The effect of alpha-1-adrenoreceptor agonist and antagonist administration on human upper gastrointestinal transit and motility.
To explore the role of alpha-1-adrenoreceptor-mediated pathways on human upper gut motor function in vivo, we studied the effects of the alpha-1-agonist phenylephrine and the alpha-1-antagonist thymoxamine on oro-caecal transit and antroduodenal motor activity. Transit was measured using a standard exhaled-breath hydrogen method, and motility was measured by intraluminal manometry. Oro-caecal transit was unaffected by 80 mg thymoxamine [median 63 min (range 35-164 min) vs. control, 65 min (range 30-155 min), P greater than 0.1]. However, phenylephrine (2.4 micrograms/kg/min) consistently delayed oro-caecal transit time to 103 min (50-215 min), P greater than 0.005. Co-administration of thymoxamine abolished this phenylephrine-induced delay. The mean amplitude of antral postprandial contractions was reduced by phenylephrine from 29 (13-37) to 10 (3-13) mmHg (P less than 0.02). In contrast, neither the pattern nor the mean inter-contraction interval was altered. Responses to phenylephrine in the duodenum were similar to those in the antrum, with reduction in amplitude from 12 (3-18) to 6 (5-13) mmHg without alteration in the pattern or interval between contractions. Nutrient transit through the upper gut can thus be inhibited via activation of an alpha-1-adrenoreceptor-mediated pathway. Failure of alpha-1-antagonist administration to alter oro-caecal transit suggests that this pathway is not tonically active, and it is therefore unlikely to play a major role in nutrient passage under normal circumstances.
Adrenergic alpha-Agonists↗
Small intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome.
CONTEXT: Irritable bowel syndrome (IBS), which affects 11% to 14% of the population, is a puzzling condition with multiple models of pathophysiology including altered motility, visceral hypersensitivity, abnormal brain-gut interaction, autonomic dysfunction, and immune activation. Although no conceptual framework accounts for all the symptoms and observations in IBS, a unifying explanation may exist since 92% of these patients share the symptom of bloating regardless of their predominant complaint. EVIDENCE ACQUISITION: Ovid MEDLINE was searched through May 2004 for relevant English-language articles beginning with those related to bloating, gas, and IBS. Bibliographies of pertinent articles and books were also scanned for additional suitable citations. EVIDENCE SYNTHESIS: The possibility that small intestinal bacterial overgrowth (SIBO) may explain bloating in IBS is supported by greater total hydrogen excretion after lactulose ingestion, a correlation between the pattern of bowel movement and the type of excreted gas, a prevalence of abnormal lactulose breath test in 84% of IBS patients, and a 75% improvement of IBS symptoms after eradication of SIBO. Altered gastrointestinal motility and sensation, changed activity of the central nervous system, and increased sympathetic drive and immune activation may be understood as consequences of the host response to SIBO. CONCLUSIONS: The gastrointestinal and immune effects of SIBO provide a possible unifying framework for understanding frequent observations in IBS, including postprandial bloating and distension, altered motility, visceral hypersensitivity, abnormal brain-gut interaction, autonomic dysfunction, and immune activation.
Anti-Bacterial Agents↗
Gallbladder motility and functional gastrointestinal disorders.
Functional gastrointestinal disorders can be defined as 'a variable combination of chronic or recurrent gastrointestinal symptoms not explained by structural or biochemical abnormalities'. Motor disorders are considered to be one of the pathogenetic mechanisms of these symptoms; in fact, it has been hypothesized that the smooth muscle of the whole gastrointestinal tract could be involved. Gallbladder motility has been evaluated in patients with dysmotility-like dyspepsia, irritable bowel syndrome and biliary disorders without gallstones; results of these observations are often inconclusive, conflicting and not always useful from a clinical point of view. The aim of this review is to explore the relationship between gallbladder motility and functional gastrointestinal disorders from pathogenetic and physiopathological points of view, and also to define the possible impact of these observations on clinical practice.
Acalculous Cholecystitis↗
Ghrelin and melatonin in the regulation of pancreatic exocrine secretion and maintaining of integrity.
Ghrelin and melatonin are produced in the central nervous system and in the gastrointestinal tissues; ghrelin in the stomach, and melatonin - in the liver and in the intestine. Both ghrelin and melatonin have been reported to protect the gastric mucosa against acute lesions and to influence gastrointestinal motility and secretions, however the physiological significance of these peptides in the gastrointestinal tissues remains unknown. In spite of the presence of ghrelin and melatonin receptors in the pancreatic tissue little is known about the role of these peptides in the pancreas. It is very likely that both ghrelin and melatonin, which are released from the gastrointestinal tract in relation to food ingestion, could be implicated in the postprandial stimulation of pancreatic enzyme secretion though the activation of cholinergic entero-pancreatic reflex and CCK release. Our experimental studies have shown that exogenous melatonin, as well as this produced endogenously from its precursor; L-tryptophan, strongly stimulates pancreatic amylase secretion when given intraperitoneally, or into the gut lumen. Intraduodenal administration of ghrelin also increases pancreatic enzyme secretion. This was accompanied by significant increases of CCK plasma levels. Above pancreatostimulatory effects of luminal administration of melatonin or ghrelin were completely reversed by bilateral vagotomy, capsaicin deactivation of sensory nerves or pretreatment of the rats with CCK1 receptor antagonist; tarazepide. Our previous findings have revealed that melatonin, as well as its precursor; L-tryptophan, effectively protects the pancreas against the damage induced by caerulein overstimulation. The beneficial effects of melatonin and L-tryptophan on the pancreas have been related to the ability of melatonin to scavenge the radical oxygen species (ROS), to activate antioxidative enzymes and to modulate the cytokine production. It has been previously shown that systemic application of ghrelin attenuated acute pancreatitis activating the immune defense mechanisms. Our recent data demonstrate that ghrelin is able to prevent pancreatic inflammatory damage though the activation of central nervous mechanisms leading to the improvement of antioxidative properties of pancreatic tissue. The results of experimental studies indicated that melatonin and ghrelin could take a part in the protection of pancreatic tissue against the damage under physiological conditions.
Animals↗
[Role of the autonomous nervous system in the regulation of the transit, absorption and storage of nutriments].
The possible role of the autonomic nervous system (ANS) in nutrition must be reevaluated in view of recent experimental data. The ANS plays a major part in both initiating and maintaining peristalsis and in coordinating gastrointestinal motility. Intestinal absorption involves extra-epithelial mechanisms such as motility and vasomotricity of the digestive tract. In addition, the ANS (sympathetic fibres) might act directly on enterocytes, or indirectly via the intestinal plexuses through a glucose-dependent mechanism. The control of exocrine and endocrine secretions depends partly on the ANS. In particular the mucous mechanoreceptors, chemoreceptors and thermoreceptors located in the intestinal area supply the sensory information needed in that kind of regulation. The efferent fibres of the ANS intervene in the control of storage of carbohydrates in the liver and of lipids in brown adipose tissue. On the other hand, gastrointestinal afferents might be implicated in this mechanism through the hypothalamic ventro-median nucleus. Finally, these data are consistent with a modern conception suggesting that the ANS is largely involved in the regulation of visceral motility, homeostasis and alimentary behaviour.
Adipose Tissue, Brown↗
Gastrointestinal manometric findings in a patient with total intestinal aganglionosis.
BACKGROUND/PURPOSE: The authors studied gastrointestinal motility in a patient with total intestinal aganglionosis (TIA) and the effect of octreotide (OCT) on ileal motility in this patient. METHODS: The 3200-g girl received ileostomy at 50 cm proximal to the ileocecal site and jejunostomy at 15 cm distal to the ligament of Treitz because of severe ileus owing to TIA. Histology of the intestines, including jejunostomy, showed no ganglion cells. Gastro-duodeno-jejunal and distal ileal manometries were done 8 months after birth. RESULTS: In upper gastrointestinal manometry, sporadic contractions and clusters consisting of 3 to 5 contractions were observed in the duodenum and jejunum, but no typical phase 3 was observed during the 3-hour recording period. In ileal manometry, long-lasting repetitive contractions were recorded at 2 distal sites. In the most proximal ileum, the frequency of contractions was less than in the 2 distal sites. OCT administration induced a decrease in the amplitude of contractions during the first 20 minutes. The amplitude increased thereafter and reached a level higher than that before OCT administration. CONCLUSIONS: In this patient, the predominant manometry finding was the remarkable hypermotility of the ileum. OCT induced a transient decrease in ileal motility and an increase in motility thereafter.
Digestive System Abnormalities↗
Motility of the gastrointestinal tract and gallbladder during long-term total parenteral nutrition in dogs.
BACKGROUND: The motility of the gastrointestinal tract during total parenteral nutrition (TPN) remains poorly understood. The objective of this study was to determine the motility pattern not only in the gastrointestinal tract but also in the gallbladders of dogs maintained by TPN. METHODS: Central venous catheters were inserted through the external jugular vein of 5 dogs and 6 strain gauge force transducers were sewn to the stomach, small intestine, and gallbladder. Two weeks later, oral food was discontinued and motility was recorded for 24 hours after the first migrating motor complex (MMC) was confirmed in the stomach as pre-TPN. TPN was started and continued for 4 weeks, and patterns of motor activity during TPN were recorded for 24 hours at the end of each week. RESULTS: The durations of MMC in the stomach, duodenum, and gallbladder in pre-TPN were 118 +/- 3 minutes, 118 +/- 2 minutes, and 118 +/- 2 minutes, respectively, but in the first week of TPN they were 432 +/- 56 minutes, 431 +/- 56 minutes, and 386 +/- 29 minutes, respectively. TPN times were significantly longer than those of pre-TPN (corrected p < .005). The durations of MMC in jejunoileum did not alter between pre-TPN and TPN. The occurrences of phase III in the stomach, duodenum, and gallbladder in pre-TPN were 12/d, but during TPN they were reduced significantly (corrected p < .005). CONCLUSIONS: TPN did not affect the motility of the jejunoileum but did inhibit the motor activities of the stomach, duodenum, and gallbladder. The inhibition of gallbladder contraction observed during TPN may be one of the factors inducing gallbladder disease.
Animals↗
Nutritional implications of cephalic phase gastrointestinal responses.
Palatable cephalic stimuli induce a simultaneous activation of gastrointestinal motility, gastric acid and pancreatic enzyme secretion, as well as, release of the gastrointestinal hormones gastrin and pancreatic polypeptide. Cholinergic neural input is the dominant mediator of these responses with cholecystokinin and gastrin acting as additional stimulatory modulators. Central cholinergic circuits, neuropeptide Y, and thyrotropin releasing hormone are candidate central stimulators of the cephalic phase. There are good arguments for glucagon-like peptide-1 and peptide YY to be physiological inhibitors of cephalic-phase responses with these peptides being released in the intestinal phase of digestion and putatively contributing to termination of the cephalically stimulated pattern. Cephalic-phase responses are used clinically as diagnostic tests to assess completeness of selective proximal vagotomy and to explore autonomic neuropathy. Pancreatic polypeptide secretion with sham feeding is an appropriate test of abdominal vagal function. Cephalically stimulated motor and secretory activity contribute greater than 50% of overall postprandial responses. Pharmacological inhibition of cephalic-vagal stimulation, resulting in reduced food intake, may be a novel approach to obesity management. Glucagon-like peptide-1 is a particular candidate because it inhibits the cephalic phase of digestion, diminishes food intake, and reduces the glycemic excursion after a meal by retarding gastric emptying, stimulating insulin and lowering glucagon release.
Animals↗
Nutritional consequences of intestinal bacterial overgrowth.
The bacterial overgrowth syndrome occurs when there are alterations in intestinal anatomy, gastrointestinal motility, or a lack of gastric acid secretion. Clinically, patients present with nonspecific gastrointestinal symptoms that include abdominal pain, bloating, excessive gas production, diarrhea, weight loss, and malabsorption. The nutritional consequences of intestinal bacterial overgrowth include vitamin deficiencies, fat malabsorption, and malnutrition. The diagnosis requires a high index of clinical suspicion and can be established by specialized testing, such as the 1-gram 14C-xylose breath test. The goal of treatment is eradication of the bacterial overgrowth (usually with antibiotics) and the correction of nutritional deficiencies.
Bacterial Infections↗
Involvement of endogenous CCK and CCK1 receptors in colonic motor function.
Cholecystokinin (CCK) is a brain-gut peptide; it functions both as a neuropeptide and as a gut hormone. Although the pancreas and the gallbladder were long thought to be the principal peripheral targets of CCK, CCK receptors are found throughout the gut. It is likely that CCK has a physiological role not only in the stimulation of pancreatic and biliary secretions but also in the regulation of gastrointestinal motility. The motor effects of CCK include postprandial inhibition of gastric emptying and inhibition of colonic transit. It is now evident that at least two different receptors, CCK(1) and CCK(2) (formerly CCK-A and CCK-B, respectively), mediate the actions of CCK. Both localization and functional studies suggest that the motor effects of CCK are mediated by CCK(1) receptors in humans. Since CCK is involved in sensory and motor responses to distension in the intestinal tract, it may contribute to the symptoms of constipation, bloating and abdominal pain that are often characteristic of functional gastrointestinal disorders in general and irritable bowel syndrome (IBS), in particular. CCK(1) receptor antagonists are therefore currently under development for the treatment of constipation-predominant IBS. Clinical studies suggest that CCK(1) receptor antagonists are effective facilitators of gastric emptying and inhibitors of gallbladder contraction and can accelerate colonic transit time in healthy volunteers and patients with IBS. These drugs are therefore potentially of great value in the treatment of motility disorders such as constipation and constipation-predominant IBS.
Animals↗
Quality of life in a US national sample of adults with diabetes and motility-related upper gastrointestinal symptoms.
Our objective was to describe the health-related quality of life (HRQoL) of individuals with diabetes with and without motility-related upper gastrointestinal symptoms compared to individuals without diabetes. A total of 483 individuals with diabetes and 422 age- and gender-matched nondiabetic controls were recruited from a prior US national health survey for a telephone interview on upper gastrointestinal symptoms. Individuals with diabetes self-reported a physician's diagnosis of diabetes and provided confirming information on clinical management measures. Subjects were asked about upper gastrointestinal symptoms in the month before interview using an instrument with demonstrated high reliability. HRQoL was measured using the SF-12 Health Survey. Individuals with diabetes reporting upper gastrointestinal symptoms scored significantly lower in HRQoL measures of physical health and mental health than either individuals with diabetes who did not report upper gastrointestinal symptoms or individuals without diabetes (P < 0.0001). Individuals with diabetes and no upper gastrointestinal symptoms had physical and mental health summary scores similar to those of individuals without diabetes. Early satiety was the strongest predictor (P < 0.0001) of differences in physical health scores between individuals with and without diabetes. Nausea was the strongest predictor (P < 0.0001) of differences in mental health scores between individuals with and without diabetes. In conclusion, this is the first US national survey to demonstrate that motility-related upper gastrointestinal symptoms are associated with a significantly lower quality of life in individuals with diabetes.
Adult↗