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PubMed1986

Gastroparesis after radiation. Successful treatment with carbachol.

Following abdominal radiation, a 16-year-old male developed persistent vomiting, metabolic alkalosis, and cachexia secondary to gastric stasis, atony, and dilatation in the absence of mechanical obstruction. Fluoroscopically and manometrically, antral motility was found to be severely impaired. Antral motor activity was not influenced by metoclopramide, but stimulated by carbachol. During oral maintenance carbachol therapy, gastric emptying of food was restored and sufficient oral nutrition could be resumed. The improvement persisted even after termination of therapy four months later. Systematic investigations on the effects of abdominal radiation on gastrointestinal motility appear to be necessary.

Adolescent↗
PubMed1985

Sympathetic preganglionic efferent and afferent neurons mediated by the greater splanchnic nerve in rabbit.

Motion sickness, a multisymptom disorder characterized by abnormal gastrointestinal motility and emesis, can be induced by vestibular effects on the sympathetic portion of the autonomic nervous system. However, the vestibular-autonomic pathways are unknown. As a first step in the analysis, we identified the locus of preganglionic sympathetic neurons (PSNs) and dorsal root afferent ganglionic neurons (DRGs) which supply sympathetic innervation to major portions of the gastrointestinal tract in the rabbit. Retrograde labeling of neurons was obtained by application of horseradish peroxidase (HRP) to the cut end of the greater splanchnic nerve. Labeled PSNs were found, ipsilaterally, within the T1 to T11 spinal cord segments, with the highest density of neurons in T6. Most PSNs were located within the intermediolateral column (IML), but a significant portion also occurred within the lateral funiculus (LF), the intercalated region (IC) and the central autonomic area (CA). The proportion of labeling between the four regions depended on the spinal cord segment. In the midthoracic levels, the distribution of labeled neurons was denser in the IML and LF, and in the caudal thoracic segments, the majority were localized in the IC and CA. Labeled cells in these four areas varied morphologically from large fusiform neurons in the IC to small fusiform neurons in the LF, small stellate neurons in the CA, and medium-size stellate neurons in the IML. The DRGs were labeled in thoracic segments T1 to T12, with the majority between T5 and T11. These labeled DRG somata of the greater splanchnic nerve were smaller in comparison with unlabeled ones.

Animals↗
PubMed2004

Function of opioids in the enteric nervous system.

Alterations in gastrointestinal motility and secretion underlie the constipating action of therapeutically administered opiates. The prototype opiate is morphine, which acts to delay gastric emptying and intestinal transit, to suppress intestinal secretion of water and electrolytes and to suppress transport of bile into the duodenum. The effects of opiates, synthetic opioids and endogenously released opioid peptides on these organ-level gastrointestinal functions reflect actions on electrical and synaptic behaviour of neurones in the enteric nervous system. Adverse effects and positive therapeutic effects of administration of opioid-receptor-blocking drugs on the digestive tract must be understood in the context of the neurophysiology of the enteric nervous system and mechanisms of neural control of gastrointestinal smooth muscle, secretory glands and blood-lymphatic vasculature. We review here the integrated systems of physiology and cellular neurobiology that are basic to understanding the actions of opioid agonists and antagonists in the digestive tract.

Animals↗
PubMed2002

Enteric nerves and interstitial cells of Cajal are altered in patients with slow-transit constipation and megacolon.

BACKGROUND & AIMS: A variety of gastrointestinal motility disorders have been attributed to alterations of interstitial cells of Cajal and malformations of the enteric nervous system. This study evaluates both the distribution of interstitial cells of Cajal and the pathohistology of the enteric nervous system in 2 severe human colorectal motility disorders. METHODS: Colonic specimens obtained from patients with slow-transit constipation (n = 11), patients with megacolon (n = 6), and a control group (n = 13, nonobstructing neoplasia) were stained with antibodies against c-kit (marker for interstitial cells of Cajal) and protein gene product 9.5 (neuronal marker). The morphometric analysis of interstitial cells of Cajal included the separate registration of the number and process length within the different regions of the muscularis propria. The structural architecture of the enteric nervous system was assessed on microdissected whole-mount preparations. RESULTS: In patients with slow-transit constipation, the number of interstitial cells of Cajal was significantly decreased in all layers except the outer longitudinal muscle layer. The myenteric plexus showed a reduced ganglionic density and size (moderate hypoganglionosis) compared with the control group. Patients with megacolon were characterized by a substantial decrease in both the number and the process length of interstitial cells of Cajal. The myenteric plexus exhibited either complete aganglionosis or severe hypoganglionosis. CONCLUSIONS: The enteric nervous system and interstitial cells of Cajal are altered concomitantly in slow-transit constipation and megacolon and may play a crucial role in the pathophysiology of colorectal motility disorders.

Adult↗
PubMed2002

Distribution and effects of PACAP, VIP, nitric oxide and GABA in the gut of the African clawed frog Xenopus laevis.

The distribution and possible effects on gastrointestinal motility of pituitary adenylate cyclase-activating polypeptide (PACAP), vasoactive intestinal polypeptide (VIP), nitric oxide and gamma-amino-butyric acid (GABA) were investigated in the African clawed frog (Xenopus laevis) using immunohistochemistry and in vitro strip preparations. PACAP- and VIP-immunoreactive nerve fibres were common in the myenteric plexus as well as in the longitudinal and circular muscle layers all along the gastrointestinal tract. Double labelling demonstrated a close correlation between PACAP and VIP immunoreactivities, indicating that the two neurotransmitters are colocalised within the enteric nervous system. Occasionally, PACAP- and VIP-positive nerve cell bodies were seen in the myenteric or submucous plexa. In addition, VIP immunoreactivity coexisted with helospectin immunoreactivity. Nitric oxide synthase (NOS)-immunoreactive nerve cells were found in the myenteric plexus at an average density for the whole gastrointestinal tract of 4584 +/- 540 cells cm(-2). The NOS-immunoreactive nerve cells were usually multipolar with an average size of 11.3 +/- 3.7 x 23.2 +/- 6.6 microm. Some NOS-immunoreactive nerve fibres were VIP-immunoreactive but not all VIP-positive fibres showed NOS immunoreactivity. GABA immunoreactivity was found in nerve fibres and nerve cells in the myenteric plexus of all regions of the gut. Few GABA-immunoreactive nerve fibres were VIP-immunoreactive. PACAP 27, VIP, sodium nitroprusside (a nitric oxide donor; NaNP) and GABA caused similar responses on spontaneously contracting circular preparations of the cardiac stomach of X. laevis. The mean force developed was decreased, mainly by a reduction in resting tension, while the amplitude of contractions was not necessarily affected. The NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) increased the mean force developed, indicating a nitrergic tone in the preparations. In contrast, PACAP 27, VIP, NaNP, GABA and L-NAME had no significant effect on longitudinal strip preparations from the duodenum. These results indicate that PACAP, VIP, nitric oxide and GABA, which are known to be important inhibitory neurotransmitters in other vertebrates, are widely spread in the enteric nervous system of Xenopus laevis and may be involved in the inhibitory control of gastric motility. Although no effect of PACAP, VIP, nitric oxide or GABA on the longitudinal strips of the duodenum was seen in this study, this does not rule out the possibility that they might play an important role in controlling intestinal motility as well.

Animals↗
PubMed1989

Review article: a role for gastrointestinal prokinetic agents in the treatment of reflux oesophagitis?

Gastro-oesophageal reflux disease may result from a host of factors. Medical therapy has largely been aimed at neutralizing acid or decreasing acid production but improvement of upper-gastrointestinal motility may prove to be a valuable treatment modality as well. This paper reviews the current state of knowledge of the pathogenesis of reflux disease and concentrates upon promotility treatment with domperidone, metoclopramide and cisapride.

Animals↗
PubMed2002

Mitochondrial neurogastrointestinal encephalomyopathy: diagnostic features of two patients.

Mitochondrial neurogastrointestinal encephalomyopathy is a rare, multisystem disorder characterized by gastrointestinal dysmotility, ptosis, neurologic findings (e.g., peripheral neuropathy), leukoencephalopathy, and thin body habitus. Gastrointestinal motility studies and skeletal muscle biopsy are recommended diagnostic tools. We report two patients that highlight the diagnostic characteristics of this rare entity.

Adolescent↗
PubMed2001

Excitatory stimulation of neurons in the arcuate nucleus inhibits gastric acid secretion via vagal pathways in anesthetized rats.

It is well established that autonomic control of gastrointestinal function is modulated by central autonomic neurotransmission. In this context it has been shown that gastrointestinal motility and secretion can be modulated by exogenous neuropeptides microinjected into the paraventricular nucleus of the hypothalamus (PVN). Furthermore, there is considerable evidence suggesting that neurons projecting from the arcuate nucleus (Arc) to the PVN may be the source of endogenous neuropeptide release in the PVN. This poses the question whether stimulation of neurons in the arcuate nucleus, e.g. by an excitatory amino acid, alters gastrointestinal function. In the present study, we investigated the effect of an excitatory amino acid, kainate, microinjected into the arcuate nucleus on gastric acid secretion in urethane-anesthetized rats. Kainate (140 pmol/rat) bilaterally microinjected into the Arc induced an significant inhibition of pentagastrin (PG) stimulated (16 mg/kg per h) gastric acid secretion throughout an observation period of 120 min after microinjection. Microinjection of kainate into hypothalamic areas outside the arcuate nucleus did not modify gastric secretion. Bilateral cervical vagotomy blocked the effect of kainate injected into the Arc on PG-stimulated gastric acid secretion. These data show that gastric secretory function can be modulated by stimulation of neuronal activity in the Arc via efferent vagal pathways. The results suggest that the arcuate nucleus is a forebrain area involved in the CNS regulation of gastrointestinal function.

Anesthetics, Intravenous↗
PubMed1996

Higher prevalence of Helicobacter pylori infection in dyspeptic patients who do not have gastric phase III of the migrating motor complex.

BACKGROUND: So far, only a few and conflicting data are available about the possible correlation between Helicobacter pylori infection and disorders of gastrointestinal motility. METHODS: In the present study we have evaluated the interdigestive manometric recordings from the stomach and duodenum of 100 consecutive dyspeptic patients, to ascertain whether the absence of phase III of the migrating motor complex (MMC) might be associated with a different prevalence of H. pylori infection. All the patients who entered a protocol study for functional dyspepsia had endoscopic examinations of the upper gastrointestinal tract with at least two biopsy specimens from both the gastric antrum and corpus (for histologic evaluation, with search for Helicobacter-like organisms). Then, 240-min interdigestive manometric recordings, with evaluation of activity fronts (phase III of the MMC), starting from the stomach and the duodenum, were made. RESULTS AND CONCLUSIONS: The data obtained suggest that in patients without evidence of gastric phase III of MMC the prevalence of H. pylori colonization is significantly (P = 0.032) higher.

Adult↗
PubMed2002

Effect of acute and chronic levosulpiride administration on gastric tone and perception in functional dyspepsia.

BACKGROUND: Altered visceral perception is common in functional dyspepsia (FD). Dopaminergic pathways control gastrointestinal motility, but whether they modulate visceral sensitivity is unknown. AIM: To investigate whether levosulpiride, a D2 antagonist, modulates gastric sensitivity and compliance in dyspeptic patients. METHODS: Eight healthy subjects and 16 dyspeptic patients underwent graded gastric distensions using a tensostat. In dyspeptic patients the same isotonic distensions were repeated during either levosulpiride or saline administration. Eight FD patients were evaluated after 4-week treatment with oral levosulpiride. Gastrointestinal symptoms were evaluated using a 100 mm visual analogue score. Perception was scored on a scale of 0 to 6. RESULTS: Although healthy subjects and FD patients had similar gastric compliance, FD patients tolerated lower tension levels. At the same distending tension levels, levosulpiride decreased gastric compliance and perception score (14 +/- 6% and 38 +/- 10% change, respectively; P < 0.05 vs. saline) only in FD patients. Isotonic distensions exhibited very reproducible perception. Chronic levosulpiride administration significantly reduced dyspeptic symptoms and increased discomfort threshold. CONCLUSIONS: Compared with healthy subjects, FD patients show marked gastric hypersensitivity. In FD patients levosulpiride decreased the perception of gastric distension with an action unrelated to change of gastric tone. Chronic levosulpiride administration significantly ameliorates gastrointestinal symptoms and increases the discomfort threshold.

Adult↗
PubMed2001

Indications and efficacy of botulinum toxin in disorders of the gastrointestinal tract.

In recent years, botulinum toxin type A (BT) has been found to be effective in the treatment of various spastic disorders of smooth muscle in the upper and lower gastrointestinal tract. The short-term efficacy of intrasphincteric injection of BT in achalasia is now well established, however, because of the chronic nature of the disease, patients will require repeated injections at regular intervals. In contrast, after a single injection into the anal sphincter, BT has impressively high healing rate with minimal side effects. BT remains a novel therapeutic approach in a range of other gastrointestinal motility disorders including diffuse oesophageal spasm, sphincter of Oddi dysfunction and anismus, and the list of its indications is increasing. BT seems to be safe but as its long-term effects remain unestablished, it should be used with caution in younger patients. In this review we discuss the mechanism of action, indications, efficacy and side-effects of BT with its use in various areas of gastrointestinal tract.

Botulinum Toxins, Type A↗
PubMed2002

Alpha 2-adrenoceptors in the enteric nervous system: a study in alpha 2A-adrenoceptor-deficient mice.

Mammals possess three types of alpha(2)-adrenoceptor, alpha(2A), alpha(2B) and alpha(2C). Our aim was to determine the type of alpha(2)-adrenoceptor involved in the control of gastrointestinal motility. In transmitter overflow experiments, myenteric plexus longitudinal muscle (MPLM) preparations of the ileum were preincubated with [(3)H]-choline and then superfused. The alpha(2)-adrenoceptor agonist medetomidine reduced the electrically evoked overflow of tritium from preparations taken from wild type but not alpha(2A)-adrenoceptor-knockout mice. In a second series of overflow experiments, MPLM preparations were preincubated with [(3)H]-noradrenaline and then superfused. Again medetomidine reduced the electrically evoked overflow of tritium from wild type but not alpha(2A)-knockout preparations. In organ bath experiments, medetomidine reduced electrically evoked contractions of segments of the ileum from wild type but not alpha(2A)-knockout mice. In each of these three series, phentolamine antagonized the effect of medetomidine in wild-type preparations with greater potency than rauwolscine. In conscious mice, gastrointestinal transit was assessed by means of an intragastric charcoal bolus. In alpha(2A)-knockout mice, the speed of gastrointestinal transit was doubled compared to wild-type. Medetomidine, injected intraperitoneally, slowed gastrointestinal transit in wild type but not alpha(2A)-knockout mice. We conclude that the cholinergic motor neurons of the enteric nervous system of mice possess alpha(2)-heteroreceptors which mediate inhibition of acetylcholine release, of neurogenic contractions and of gastrointestinal transit. The noradrenergic axons innervating the intestine possess alpha(2)-autoreceptors. Both hetero- and autoreceptors are exclusively alpha(2A). It is the alpha(2A)-adrenoceptor which in vivo mediates the inhibition of intestinal motility by the sympathetic nervous system.

Acetylcholine↗
PubMed1998

Constipation and diarrhea in pregnancy.

Constipation and diarrhea are common during pregnancy, occurring in up to one-third of women. Constipation is often the result of physiologic changes that occur during pregnancy, usually from hormonal effects on gastrointestinal motility. Diarrhea, on the other hand, is often caused by the same disorders responsible for diarrhea in the nonpregnant patient. The incidence, pathophysiology, evaluation, and treatment of constipation and diarrhea during pregnancy are reviewed in this article.

Constipation↗
PubMed1998

Circulating gastrointestinal hormone abnormalities in patients with severe idiopathic constipation.

OBJECTIVE: This study aimed to determine if there is an abnormality of circulating gastrointestinal hormones in patients with severe idiopathic constipation. METHODS: Twelve patients, all female (median age 34 yr) and 12 healthy controls (eight female, median age 32 yr) were studied. A radioisotope-labeled solid/liquid meal was ingested, and the serum hormone response, as well as the relationship between serum hormones and rates of gastric emptying and small intestinal transit, were studied for 180 min postprandially. RESULTS: Somatostatin levels were higher in patients with constipation (basal level, controls vs patients, 31 vs 57 pmol/L, p < 0.05, median values; peak level, 48 vs 60, p < 0.05). Patients showed a significantly lower somatostatin integrated incremental meal response (2182 vs 104, p < 0.05). No correlation was found between the somatostatin levels and rates of upper gastrointestinal transit in patients. Pancreatic glucagon was significantly decreased (p=0.04). Enteroglucagon levels were significantly lower (p > 0.05) in patients between 30 and 60 min after the meal. The peak found after the meal in normal subjects was absent. Basal levels of pancreatic glucagon correlated with small bowel transit by two different measures: head of meal (r=0.69, p=0.03) and cecal filling at the time of 50% gastric emptying (r=0.84, p=0.002). No significant differences between the two groups could be found for basal and peak levels at different times and integrated incremental response to the meal for insulin, gastric inhibitory polypeptide (GIP), glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK), gastrin, pancreatic polypeptide (PP), motilin, neurotensin, and peptide tyrosine tyrosine (PYY). CONCLUSION: Patients with severe idiopathic constipation have specific abnormalities of circulating gut hormones that most likely play a role in gastrointestinal motility and that may be of pathophysiological significance.

Acute Disease↗
PubMed1999

The autonomic nervous system in functional bowel disorders.

Communications along the brain-gut axis involve neural pathways as well as immune and endocrine mechanisms. The two branches of the autonomic nervous system are integrated anatomically and functionally with visceral sensory pathways, and are responsible for the homeostatic regulation of gut function. The autonomic nervous system is also a major mediator of the visceral response to central influences such as psychological stress. As defined, functional disorders comprise a constellation of symptoms, some of which suggest the presence of altered perception, while other symptoms point to disordered gastrointestinal function as the cause of the symptoms. A growing number of reports have demonstrated disordered autonomic function in subgroups of functional bowel patients. While a number of different methods were used to assess autonomic function, the reports point to a generally decreased vagal (parasympathetic) outflow or increased sympathetic activity in conditions usually associated with slow or decreased gastrointestinal motility, while other studies found either an increased cholinergic activity or a decreased sympathetic activity in patients with symptoms compatible with an increased motor activity. Under certain conditions, altered autonomic balance (including low vagal tone and increased sympathetic activity) may alter visceral perception. Autonomic dysfunction may also represent the physiological pathway accounting for many of the extraintestinal symptoms seen in irritable bowel syndrome patients and some of the frequent gastrointestinal complaints reported by patients with disorders such as chronic fatigue and fibromyalgia.

Autonomic Nervous System↗
PubMedDate not supplied

Effects of cisapride on abnormally prolonged endogastric alkalinity time and delayed gastric emptying in cirrhotic patients.

BACKGROUND/AIMS: An abnormally prolonged alkalinity time in endogastric long-term pH monitoring has been previously demonstrated in cirrhotic patients. Recently a growing body of evidence suggest the existence of severe abnormalities of gastric emptying in the same patients and more generally of gastrointestinal motility changes in many portal hypertensive animal models. Assuming that there was a good correlation between endogastric alkalinity and a delayed emptying of gastric bile reflux, the aim of this study was to evaluated the effect of a gastrokinetic drug, Cisapride, both on circadian gastric pH and on gastric emptying in cirrhotic patients compared with controls. MATERIALS AND METHODS: Ten in patients with chronic liver disease and portal hypertension (six males, four females, median age 49.5, range 28-59) were enrolled. The control group included twelve inpatients without cirrhosis (seven females and five males, average age 45 years, range 31-54) free from endoscopic esophagogastro-duodenal lesions. The subjects were submitted to a 24h endogastric pH monitoring and gastric emptying study before and after administration of Cisapride (10 mg tid for three days). To gastric emptying study we used an ultrasonographic method evaluating the ratio between the antropyloric region volume before and at a fixed time after a solid/liquid standard meal. RESULTS: Basal 24 h gastric pH monitoring in cirrhotic patients showed a significant prolonged time of alkalinity (pH conventionally over 4) during the entire registration and mainly in postprandial period vs controls. The same patients group showed also a delayed gastric emptying when compared to controls. Cisapride administration significantly reduced both the abnormally prolonged alkalinity time and delayed gastric emptying in cirrhotic group without affecting the same parameters in the control group. CONCLUSIONS: Cisapride significantly reduces both the delayed gastric emptying time and the abnormally prolonged alkalinity time in cirrhotic group. Taken together, the results offered an indirect evidence that abnormally prolonged alkalinity in cirrhotic patients may be due, at least in part, to changes in gastroduodenal motility leading to a reduced gastric clearance of potentially noxious duodeno-gastric alkaline reflux.

Adult↗
PubMed2002

Cisapride does not prevent postoperative vomiting in children.

UNLABELLED: The peripherally acting prokinetic drug cisapride can overcome opioid-induced gastrointestinal paresis and may thereby eliminate a stimulus for postoperative vomiting. We conducted a prospective, randomized, double-blinded, controlled trial of 96 children undergoing inguinal surgery to determine whether cisapride would reduce the incidence of postoperative vomiting after general anesthesia supplemented with morphine. Group C1 patients (n = 38) received cisapride 0.3 mg/kg orally 1 h before surgery and placebo 6 h later, Group C2 (n = 28) received cisapride both before and after surgery, and Group P (n = 30) received placebo. Mean age (5.0 +/- 2.7 yr) and weight (21.0 +/- 8.6 kg), median pain scores and parent satisfaction scores, and incidence of rescue analgesic administration were similar across groups. Contrary to our hypothesis, incidences of postoperative vomiting in the hospital (32% vs 20%, P = 0.33) and at home (53% vs 46%, P = 0.33) did not vary by treatment group (with [C1 and C2] and without [P] cisapride, respectively). There was a trend toward more severe postoperative vomiting (three or more episodes) in children who received cisapride versus those who did not, both in hospital (6% vs 0%, P = 0.3) and at home (22% vs 8%) (P = 0.13). We conclude that cisapride does not prevent postoperative vomiting in this patient population and speculate that factors other than reduced gastrointestinal motility associated with general anesthesia and opioids are more important determinants of postoperative vomiting. IMPLICATIONS: Cisapride does not prevent postoperative vomiting in children and may increase its severity.

Antiemetics↗