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PubMed2006

Differentiation potential of bone marrow stromal cells to enteric neurons in vitro.

OBJECTIVE: To investigate whether bone marrow stromal cells (BMSC) can be induced to differentiate into enteric neurons and to produce more nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF). METHODS: Bone marrow stromal cells were harvested from male Sprague-Dawley rats and cultured in Dulbecco's modified eagle medium supplemented with 20% fetal bovine serum. The BMSC were passaged six times and characterized by flow cytometry. The BMSC were pre-induced by basic fibroblast growth factor (10 ng/mL) for 24 h, then induced with GDNF in fetal gut condition medium (FGCM) for 10 days. The expressions of neuronal markers neural specific enolase (NSE), neurofilament (NF), glial cell marker, glial fibrillary acedic protein (GFAP), and enteric neuronal marker protein gene product 9.5 (PGP9.5), neural nitric oxide synthase (nNOS), and enteric neural transmitter vasoactive intestinal polypeptide (VIP) were detected by fluorescent immunohistochemistry. Expression levels of GDNF and NGF mRNA were determined by RT-PCR. RESULTS: The cultured BMSC were CD90 (99.7%) positive and CD45 negative on flow cytometry. At day 10 of induction, 58.5 +/- 10.8% cells adopted neuron-like morphological changes and showed expression of NSE (47.6 +/- 7.5%), NF (75.6 +/- 8.4%), GFAP (negative), PGP9.5 (57.7 +/- 6.5%), nNOS (46.6 +/- 5.4%) and VIP (72.3 +/- 6.7%) by immunofluorescence. The BMSC expressed low levels of NGF and GDNF mRNA; however, after induction of GDNF in FGCM, the expression levels of NGF and GDNF mRNA were significantly increased. CONCLUSION: Bone marrow stromal cells have the potential to be induced to differentiate into enteric neurons, express enteric neural transmitters, and produce more NGF and GDNF. Therefore, BMSC could be used as new method to treat gastrointestinal motility disorders associated with enteric neural lesions.

Animals↗
PubMed1996

Neoral (cyclosporin) in dermatology: technical aspects.

Cyclosporin is a highly effective treatment for psoriasis, atopic dermatitis and many other inflammatory dermatoses. Absorption of cyclosporin from the traditional Sandimmun formulation is influenced by many factors, including bile flow, food and gastrointestinal motility. As a consequence, the bioavailability of Sandimmun is low and highly variable, both within and between patients. Neoral is a microemulsion preconcentrate formulation that has self-emulsifying properties and immediately forms a microemulsion in aqueous fluids, allowing rapid and consistent absorption of cyclosporin from the gastrointestinal tract. Benefits in dermatology are likely to be more patients responding at lower doses, a faster onset of action and a more predictable response to a given dose allowing for fewer dose adjustments. In the future these benefits of Neoral may lead to the simplified management of cyclosporin treatment and less frequent safety monitoring.

Chemistry, Pharmaceutical↗
PubMed2004

The gastrointestinal pharmacology of cannabinoids: an update.

Recent work in the field of gastrointestinal pharmacology of cannabinoids has focused on enteric endocannabinoid and endovanilloid systems and their modulation in pathophysiological conditions. CB(1) receptor immunoreactivity was detected on enteric cholinergic neurones and vasoactive intestinal peptide-containing submucosal ganglion cells, on discrete nuclei of the dorsovagal complex (involved in emesis) and on central and peripheral vagal terminals, thus controlling gastroesophageal reflux and gastrointestinal motility. CB(1) receptor activation by endocannabinoids inhibited induced fluid secretion and inflammation in animal models and reduced proliferation of cultured colorectal cancer cells. Endocannabinoids also activate cannabinoid CB(2) and vanilloid VR1 receptors in certain inflammatory states. Thus endocannabinoid metabolism could provide a useful therapeutic target for many gastrointestinal disorders.

Animals↗
PubMed2005

Review article: The role of serotonergic agents in the treatment of patients with primary chronic constipation.

Chronic constipation is a highly prevalent disorder that is associated with significant direct and indirect costs and has substantial impact on patient quality of life. It is more common among women and non-white populations and is evenly distributed across adult age groups. Constipation is a heterogeneous disorder associated with multiple symptoms and aetiologies. Recent research has increased our understanding of the pathogenesis of this disorder and the central role of the neurotransmitter serotonin in mediating gastrointestinal motility, secretion and sensation. Abnormal serotonin signalling and reuptake appear to play central roles in the symptoms of a subset of patients with chronic constipation. This observation provides a rationale for the use of targeted serotonergic agents for the treatment of chronic constipation. As the role of serotonin in gastrointestinal function is further elucidated and additional candidate drugs are developed, it is likely that serotonergic agents will afford additional treatment options for patients with chronic constipation. This article provides a concise review of the evidence supporting a role for serotonin in the pathogenesis of chronic constipation and a summary of the currently available evidence supporting the use of serotonergic agents for this disorder.

Brain↗
PubMedDate not supplied

Physiology of the aerodigestive system and aberrations in that system resulting in aspiration.

BACKGROUND: Aspiration pneumonia remains a significant and often devastating problem in critically ill patients. It is unclear whether aspiration pneumonia occurs because of problems in the handling of oropharyngeal secretions or if the reflux of gastric contents is the major etiological factor. Additionally, the obvious breakdown of upper aerodigestive protective mechanisms in the critically ill patient population is largely unstudied. Finally, the impact and contribution of tubes, both endotracheal and nasoenteral, on aspiration pneumonia is unclear. METHODS: A Medline literature search on scientific and review articles concerning the normal physiology of the aerodigestive tract and factors that compromised normal physiology was undertaken. Readings were supplemented by expert outside opinion from researchers in these fields and from the combined expertise from a multidisciplinary panel of experts assembled at a recent summit on aspiration pneumonia. RESULTS: Changes in the normal physiology of the aerodigestive tract are vast and varied and dependent on the response to injury, iatrogenic interventions, and the use of nasoenteral and endotracheal tubes. The effects on gastric and esophageal motility are likely dynamic and represent an ongoing but changing risk of reflux for the patient. Nasoenteral and endotracheal tubes likely compromise upper aerodigestive protective mechanisms. CONCLUSIONS: More research is needed on the functioning of the aerodigestive protective mechanisms in critically ill patients. Understanding of the dynamic changes in gastrointestinal motility will also be an important factor to decrease the incidence of aspiration pneumonia in this patient population.

Digestive System↗
PubMed1995

Long QT syndrome during high-dose cisapride.

The gastrointestinal prokinetic drug, cisapride, is widely used for the treatment of diabetic gastroparesis and disorders of gastrointestinal motility. We present a case of acquired QT prolongation, syncope, and nonsustained ventricular tachycardia associated with high doses of cisapride.

Cisapride↗
PubMed1994

The motilin gene: subregional localisation, tissue expression, DNA polymorphisms and exclusion as a candidate gene for the HLA-associated immotile cilia syndrome.

The product of the human motilin gene (MLN) has an important role in regulating gastrointestinal motility. The precise chromosomal localisation and expression of this gene are still unresolved. Here, we report a detailed study assigning MLN to 6p21.3; MLN is tightly linked to the HLA-DQalpha locus. Moreover, MLN expression has been evaluated in a large series of tissues. Positive signals have been obtained for brain, bronchi and a gastrointestinal malignancy. Direct sequencing exon by exon of the codifying region, intron/exon boundaries and promoter has allowed the identification of three DNA polymorphisms, one of which corresponds to a common protein variant. The chromosomal localisation of MLN, and its expression in broncoepithelial cells suggests that this gene is involved in immotile-cilia syndrome (ICS) disease. Sequence and segregation analysis of the MLN gene carried out in two families, in which the disease locus was previously assigned to 6p21.3, exclude MLN as a candidate gene for the HLA-associated form of ICS.

Base Sequence↗
PubMed2000

[Protection of the mucosal barrier by nutritional strategies. What are the therapeutic options?].

The dysfunction of intestinal barrier allows the translocation of both endotoxin and whole bacterial organisms. It plays an important role in the development of multiple organ failure (MOF). The mucosa ia one component of this barrier. Trauma, atrophy and the "systemic inflammatory response syndrome" increase gastrointestinal permeability. These abnormalities may contribute to the pathophysiology of sepsis. Malnutrition per se compromises the gut's barrier function. Maintenance of gastrointestinal blood flow may be facilitated by (glutamine-enriched?) enteral diets. The most important conclusions of the majority of controlled trials support the concept of the very early enteral nutrition (within 24 hours after trauma): the outcome of seriously ill patients is improved, the rate of complications and infections is reduced. Gastrointestinal motility disorders may interfere with the initiation and tolerance of early enteral nutrition. They may be managed by prokinetic agents (cisapride, erythromycin) or by bypassing the stomach with a nasoenteric tube.

Gastrointestinal Diseases↗
PubMed1999

Beneficial effects of NSAIDs in the gastrointestinal tract.

Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin exert irritant and toxic effects upon the organs of the gastrointestinal tract. NSAID toxicity in the gastrointestinal tract is related, at least in part, to the inhibition of the cyclo-oxygenase (COX) enzyme, leading to a reduction of 'cytoprotective' prostaglandin synthesis. In this paper, examples in which NSAIDs exert beneficial effects in the gastrointestinal tract are discussed. NSAIDs, particularly aspirin, are showing promise in the chemoprevention of colorectal, and, to a lesser degree, oesophageal cancers. The clinical value of NSAIDs in the treatment of established gastrointestinal tract cancers is also worthy of further study. There is good clinical evidence showing the value of diclofenac for the treatment of biliary colic and aspirin or ibuprofen for the prevention of gallstones. NSAIDs also have therapeutic potential against other inflammatory gastrointestinal diseases in the oesophagus and possibly pancreas and liver. To a lesser degree, there is some evidence that NSAIDs may have a therapeutic potential in certain gastrointestinal motility disorders, such as aspirin in the post-irradiation syndrome. It therefore follows that in these cancerous, inflammatory and motility pathologies, prostaglandins exert deleterious effects. The paradox of prostaglandins being 'cytoprotective' and potentially damaging can be explained by considering the enzymic origin of prostaglandins. COX-1 is expressed physiologically while inducible COX-2 is expressed in pathological situations. The beneficial clinical effects of selective COX-2-inhibiting NSAIDs in the gastrointestinal tract deserve further study. This paper challenges the concept of 'cytoprotection'.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1989

Rationale for the development of a novel gastrointestinal prokinetic, cisapride.

Several promotility drugs have been used to correct disorders caused by disturbed gastrointestinal motility. However these drugs have various drawbacks. Their effects on smooth muscle activity may be restricted to part of the digestive system, or may not be very efficient. On the other hand, their use is somewhat limited by side effects: drugs may not be specific for the motor functions of the gastrointestinal tract or not even for the gastrointestinal tract itself. The desirability of improving the promotility effects and eliminating the secondary effects of existing drugs constituted the rationale for developing cisapride. This aim was achieved by influencing--in a physiological way--the release of acetylcholine, the main neurotransmitter in the 'gut brain', the myenteric plexus.

Cisapride↗
PubMed2001

5-hydroxytryptamine and the gastrointestinal migrating motor complex.

The migrating motor complex (MMC) is the basic cyclic pattern of gastrointestinal motility that is observed in the interdigestive periods in humans as well as in monogastric animals. Among the mediators involved in its regulation, an increasing number of reports point out that 5-hydroxytryptamine (5-HT) has a pivotal role. Taking into account that this pattern is disturbed in patients suffering from several gastrointestinal disorders, studies leading to a better understanding of 5-HT actions have special relevance. This article reviews the current knowledge on the role of 5-HT receptors in the control of the MMC.

Animals↗
PubMed1999

Central gastrin inhibits feeding behavior and food passage in neonatal chicks.

The gastrin/cholecystokinin (CCK) family is recognized as the principal family of hormones involved in regulation of the gastrointestinal tract CCK is recognized as a satiety hormone in mammalian species, but it has been suggested that gastrin rather CCK may have an important role in controlling feeding behavior in the neonatal chick through a poorly developed blood brain barrier. So far, however, there is no direct evidence that central gastrin inhibits food intake in neonatal chicks. The aim of this study was to elucidate whether central administration of gastrin 1) inhibits feeding behavior and 2) alters food passage from the crop. The effects of central administration of gastrin on food intake were investigated in experiment 1. Birds (2-day-old) were food-deprived for 3 h and then gastrin or saline was injected intracerebroventricularly. Gastrin strongly inhibited food intake in a dose-dependent fashion for 2 h. Thereafter, the effects of central gastrin on feeding behavior and serum corticosterone concentration were examined in experiment 2. Following central administration of gastrin, food intake was depressed and pecking behavior was inhibited. Serum corticosterone concentration was not altered by central administration of gastrin. The influence of central gastrin on food passage from the crop was investigated in experiment 3. Central administration of gastrin clearly delayed food passage. In conclusion, central gastrin appears to have a strong effect for the satiety and gastrointestinal motility in the neonatal chick.

Animals↗
PubMed2001

Proximal gastric motor and sensory function in slow transit constipation.

BACKGROUND: Slow transit constipation may be part of a more generalized gastrointestinal motility disorder. METHODS: Gastric motor and sensory function were evaluated using a barostat in 17 patients with slow transit constipation and in 16 healthy controls. A step-wise isobaric distension procedure was performed, followed by a barostat procedure including a liquid meal. Symptoms were scored using visual analog scales. Plasma levels of gastrointestinal hormones were determined postprandially. RESULTS: Proximal gastric compliance was significantly reduced in the patients. Basal gastric volume did not differ between patients and controls. Postprandial fundus relaxation was significantly reduced in the patients and correlated significantly with daily upper gastrointestinal symptoms. Postprandial secretion of cholecystokinin and gastrin was reduced in the patients. CONCLUSIONS: In patients with slow transit constipation, proximal gastric compliance is reduced and postprandial fundus relaxation is impaired. These findings support the hypothesis that slow transit constipation may be part of a pan-enteric disorder.

Adult↗
PubMed2004

Autonomic dysfunction and gastroparesis in cirrhosis.

BACKGROUND: Patients with cirrhosis of the liver frequently present with many gastrointestinal complaints that are most likely due to abnormal gastrointestinal motility. The cause of these motility disorders in cirrhotics is unknown, however, underlying autonomic dysfunction may play a role. OBJECTIVE: To determine the association between autonomic dysfunction and delayed gastric emptying in cirrhotic patients. METHODS: We prospectively studied 20 patients with cirrhosis of the liver and postprandial abdominal pain, nausea, and vomiting and 10 asymptomatic patients with Hepatitis C (HCV) and no evidence of cirrhosis. All patients underwent 5 standardized cardiovascular tests to assess autonomic function. Each test was scored on a continuum from 0 (normal) to 5 (severe disease), thus producing a composite score of 0 to 5 for each subject. A composite score of greater than 1.5 was considered abnormal, with 5 representing severe autonomic involvement. A solid phase gastric emptying study was performed in each patient and a gastric retention of greater than 50% at 100 minutes was considered abnormal. RESULTS: The mean percent retention at 100 minutes was 70.7% in the cirrhotic group vs. 26.1% (P < 0.001) in the patients with HCV and no evidence of cirrhosis (controls). The composite autonomic score for the cirrhotic group was 3.4 vs. 1.2 (P < 0.001) in the controls. CONCLUSIONS: Our results suggest that gastroparesis is common in patients with cirrhosis of the liver, and may account for gastrointestinal symptoms of postprandial abdominal pain, nausea, and vomiting. The presence of autonomic dysfunction correlates positively with underlying motility disorders, such as delayed gastric emptying.

Adult↗
PubMed2002

Influence of prokinetics on the gastrointestinal transit and residence times of activated charcoal.

OBJECTIVE: To find the effects of prokinetics, saline cathartics and different charcoal doses on the gastrointestinal transit and residence times of activated charcoal (AC). SETTING: Five undergraduate volunteers of College of Health Sciences, Nnamdi Azikiwe University, Nnewi Campus, Anambra State, Nigeria, were studied. METHODS: After an overnight fast, the volunteers were given 10 g and 20 g AC with and without saline cathartics, in a simple cross-over design in which the subjects served as their own control. In another experiment, the volunteers received 10 g AC and magnesium sulphate, with propantheline (as bromide 15 mg), metoclopramide (as hydrochloride 10 mg), placebo liquid or identical placebo capsule. Gastrointestinal transit and residence times of AC were recorded. RESULTS: Increase in the dose of AC significantly (P < 0.05) decreased the transit, but not the residence time of AC. Addition of saline cathartics (Na2SO4 and MgSO4) decreased both the transit and residence times of AC significantly (P < 0.05). Also, administration of propantheline, but not metoclopramide, produced a significant (P < 0.05) decrease in both the transit and residence times of AC. The transit and residence times were statistically (P < 0.05) different in both the magnesium sulphate group, as well as in the placebo liquid and placebo capsule groups. CONCLUSION: Cathartic efficiency is enhanced by alteration of gastrointestinal motility with propantheline.

Adult↗
PubMedDate not supplied

Epidural and spinal anesthesia do not influence gastric emptying and small intestinal transit in volunteers.

The influence of thoracic epidural anesthesia, spinal anesthesia, and a painful stimulus on gastric emptying, orocecal transit time, and small intestinal transit were studied in nine healthy volunteers. Gastric emptying was measured by the acetaminophen absorption method. Orocecal transit time was determined by measuring end-expiratory hydrogen concentration. Small intestinal transit was calculated from measurements of the orocecal transit time and gastric emptying. Cold pain stress with intermittent immersion of the feet in ice-cold water was used as a painful stimulus. Each volunteer was investigated on four occasions: 1. during nociceptive stimulation of the feet (cold pain); 2. during low spinal anesthesia with block of the afferent nerves from the nociceptive stimulated area; 3. during thoracic epidural anesthesia (0.5% bupivacaine) with block of the efferent nerves to the stomach and small intestine but with intact afferents from the nociceptive stimulated area; 4. as a control study without pain and anesthesia. Without spinal anesthesia, immersion of the feet in cold water was very painful and caused a circulatory stress reaction with increased blood pressure. Cold pain stress in itself did not influence gastric emptying, orocecal transit time, or small intestinal transit. Neither did epidural or spinal anesthesia during cold pain stress influence these variables of gastrointestinal motility. Thus, low spinal anesthesia or thoracic epidural anesthesia in itself did not influence gastric emptying, orocecal transit, or small intestinal transit.

Adult↗
PubMed2006

Inducible nitric oxide synthase and tumor necrosis factor-alpha in delayed gastric emptying and gastrointestinal transit induced by lipopolysaccharide in mice.

Gastrointestinal motility disturbances during endotoxemia are probably caused by lipopolysaccharide (LPS)-induced factors: candidates include nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-1ss, and interleukin-6. Flow cytometry was used to determine the effects of LPS and these factors on gastric emptying (evaluated indirectly by determining percent gastric retention; %GR) and gastrointestinal transit (GIT) in male BALB/c mice (23-28 g). NO (300 microg/mouse, N = 8) and TNF-alpha (2 microg/mouse, N = 7) increased (P < 0.01) GR and delayed GIT, mimicking the effect of LPS (50 microg/mouse). During early endotoxemia (1.5 h after LPS), inhibition of inducible NO synthase (iNOS) by a selective inhibitor, 1400 W (150 microg/mouse, N = 11), but not antibody neutralization of TNF-alpha (200 microg/mouse, N = 11), reversed the increase of GR (%GR 78.8 +/- 3.3 vs 47.2 +/- 7.5%) and the delay of GIT (geometric center 3.7 +/- 0.4 vs 5.6 +/- 0.2). During late endotoxemia (8 h after LPS), both iNOS inhibition (N = 9) and TNF-alpha neutralization (N = 9) reversed the increase of GR (%GR 33.7 +/- 2.0 vs 19.1 +/- 2.6% (1400 W) and 20.1 +/- 2.0% (anti-TNF-alpha)), but only TNF-alpha neutralization reversed the delay of GIT (geometric center 3.9 +/- 0.4 vs 5.9 +/- 0.2). These findings suggest that iNOS, but not TNF-alpha, is associated with delayed gastric emptying and GIT during early endotoxemia and that during late endotoxemia, both factors are associated with delayed gastric emptying, but only TNF-alpha is associated with delayed GIT.

Animals↗
PubMed1997

Gastric myoelectrical activity in patients with diabetes. Role of glucose control and autonomic nerve function.

OBJECTIVE: Gastric myoelectrical activity was studied in diabetic patients using electrogastrography (EGG) to elucidate the relationship between glucose control, diabetic autonomic neuropathy (AN), and gastrointestinal motility. RESEARCH DESIGN AND METHODS: Cutaneous EGG was recorded during 1 h of fasting and 1 h after the ingestion of a standard meal in 57 diabetic patients and 10 healthy subjects. EGG was measured in 12 diabetic patients after glycemic control for 4 weeks. Diabetic patients were also studied with respect to the presence of gastrointestinal symptoms and AN. RESULTS: The percentage of dominant electrical frequency (DF) in normal range (the percentage ratio between the power at 2.4-3.6 cycles/min [cpm] and at 1-10 cpm) was significantly lower in patients with AN than in either the control subjects or the patients without AN (P < 0.01). The dominant frequency instability coefficient (DFIC) was significantly higher in patients with and without AN than in the control subjects (P < 0.01). The postprandial-to-fasting power ratio (PR) was the lowest in patients with AN (P < 0.01). Multiple regression analysis revealed that HbA1c levels were independently associated with the DFIC (R2 = 0.099, P = 0.0170) and that AN and HbA1c levels were independently associated with the PR (R2 = 0.378, P < 0.0001) in diabetic patients. The percentage of normal DF increased and the DFIC decreased significantly after glycemic control in 12 diabetic patients (P = 0.0409; P = 0.0096, respectively). CONCLUSIONS: There appears to be an association between improvement in gastric myoelectrical activity and autonomic nerve function. Abnormalities of gastric myoelectrical activity may be partly ameliorated via the improvement of autonomic nerve function, which accompanies glycemic control.

Adult↗