Gastric Motor Function Research Articles

The 5‐HT4 antagonist R216073 does not affect gastric motor and sensory function in patients with functional dyspepsia

Serotonin and the 5-HT4 receptor play an important role in gastrointestinal motor and sensory functions. While 5-HT4 agonists are known for their prokinetics properties, the effect of 5-HT4 antagonists on upper gastrointestinal functions is largely unknown. To assess the effect of a 5-HT4 receptor antagonist (R216073) on gastric relaxation and visceral sensitivity in patients with functional dyspepsia. Secondly, the influence of a functional polymorphism in the gene encoding the serotonin transport protein on drug response was determined. A double-blind, randomized, placebo-controlled, two-period crossover study was performed in 20 functional dyspepsia patients. The effect of a single dose of 2,000 mg R216073 on gastric relaxation and sensitivity was tested using three-dimensional ultrasonography and a nutrient drinktest. R216073 did not affect partial gastric volumes or upper abdominal sensations scored during three-dimensional ultrasonography (P > 0.05). The maximum tolerated volume or upper abdominal sensations induced by the drinktest were not affected by R216073 (P > 0.05). The serotonin transport protein promoter polymorphism was not associated with any of the end-points of the study. A single dose of R216073 had no effect on fundic relaxation, drinking capacity, or upper abdominal symptoms in patients with functional dyspepsia.

Effect of intravenous infusion of glyceryl trinitrate on gastric and small intestinal motor function in healthy humans

Glyceryl trinitrate is a donor of nitric oxide that relaxes smooth muscle cells of the gastrointestinal tract. Little is known about the effect of glyceryl trinitrate on gastric emptying and no data exist on the possible effect of glyceryl trinitrate on small intestinal transit. To examine the effect of intravenous infusion of glyceryl trinitrate on gastric and small intestinal motor function after a meal in healthy humans. Nine healthy volunteers participated in a placebo-controlled, double-blind, crossover study. Each volunteer was examined during intravenous infusion of glyceryl trinitrate 1 microg/kg x min or saline. A gamma camera technique was used to measure gastric emptying and small intestinal transit after a 1600-kJ mixed liquid and solid meal. Furthermore, duodenal motility was assessed by manometry. Glyceryl trinitrate did not change gastric mean emptying time, gastric half emptying time, gastric retention at 15 min or small intestinal mean transit time. Glyceryl trinitrate did not influence the frequency of duodenal contractions, the amplitude of duodenal contractions or the duodenal motility index. Intravenous infusion of glyceryl trinitrate 1 microg/kg x min does not induce major changes in gastric or small intestinal motor function after a 1600-kJ meal in healthy volunteers.

Gastric motor function and emptying in the right decubitus and seated body position as assessed by magnetic resonance imaging

To determine the effect of the right decubitus lying body position (RP) on relevant parameters of human gastric motor function in healthy volunteers. Postprandial gastric function after ingestion of a solid/liquid meal (150 g/150 mL) was assessed over 90 minutes in volunteers in the RP and seated position (SP). Ten healthy volunteers were imaged using two MRI systems that differed in architecture and field strength. Stomach and intragastric air volume, intragastric meal distribution, gastric emptying, and gastric peristalsis were compared between the RP and SP. Body position did not affect gastric relaxation (RP, 372 mL vs. SP, 384 mL) and initial gastric volumes (stomach: RP, 458 mL vs. SP, 462 mL; meal: RP, 377 mL vs. SP, 399 mL; intragastric air: RP, 110 mL vs. SP, 98 mL). Postprandial stomach volume and gastric activity (RP and SP, 3.1 minute(-1)) were also similar. Meal emptying showed different characteristics, resulting in a significant but small difference in meal volume of -43 mL at t = 90 minutes (P < 0.05). Gastric MRI in RP is feasible for clinical research assessing gastric motor function. The subtle difference in meal emptying may be induced by posture-dependent vagal activity. This study confirms that MRI is a highly sensitive imaging technique for assessing gastrointestinal function in humans.

The dorsal vagal complex as a site for cocaine- and amphetamine-regulated transcript peptide to suppress gastric emptying

Cocaine- and amphetamine-regulated transcript-derived peptides (CARTp) and corticotropin-releasing factor (CRF) alter feeding and gastrointestinal function after central administration, and the gastric inhibitory effects are mediated through CRF. We hypothesized that dorsal hindbrain effects of CARTp on gastric emptying are mediated by the vagus nerve and that the dorsal vagal complex (DVC) is a site of action for the gastric inhibitory effects of both CARTp and CRF. Rats were equipped with chronic intragastric fistulas and guide cannulas aimed at the fourth ventricle or the DVC. Fourth intracerebroventricular CARTp-induced suppression of 12 ml glucose (12.5%) gastric emptying during fill was blocked by subdiaphragmatic vagotomy. To establish whether the DVC may be a site of action for CARTp and/or CRF, intraparenchymal microinjections (0.25 microl) of CARTp (0.1 and 0.5 microg) and CRF (5 and 10 pmol) were administered in the DVC. Each dose, previously shown to be ineffective after fourth intracerebroventricular administration, suppressed gastric emptying during gastric fill vs. vehicle, but neither peptide changed gastric secretion volume or gastric acidity. The results indicate that the DVC is a target site for CRF and CARTp to inhibit gastric emptying and that the vagus mediates dorsal hindbrain effects of CARTp on gastric motor function.

Evaluation of the effects of mastication and swallowing on gastric motility using electrogastrography

The influence of mastication and swallowing on gastric motor function was evaluated by electrogastrography (EGG) and abdominal ultrasonography. The subjects were 30 elderly patients with tubal feeding without mastication and swallowing (T group) and 30 elderly controls who processed food by mastication and swallowing (C group). Gastric motor function was percutaneously examined before and after the ingestion of 250 ml of a liquid diet using an electrogastrograph (NIPRO EGG, A and D, Tokyo, Japan). The cross-sectional area of the gastric antrum was measured at 1 and 30 min after the start of ingestion of the liquid diet by external ultrasonography of the abdomen, and the gastric excretion function was evaluated. Furthermore, the spectral analysis of heart rate variability was performed using Holter electrocardiograms before and after ingestion. The low frequency power (LF power, 0.04-0.15 Hz), high frequency power (HF power, 0.15-0.40 Hz), and the LF/HF ratio were determined. The peak amplitude at 3 cycles per minute (cpm) was significantly increased after ingestion in the C and T groups (p<0.05), and the ratio of increase was significantly lower in the T group (p<0.05). The mean amplitude for the brady-gastria and tachy-gastria was significantly higher in the T group than in the C group (p<0.05). The gastric excretion function, as evaluated by external ultrasonography of the abdomen, was significantly lower in the T group than in the C group (p<0.05). An analysis of heart rate variability demonstrated that the HF power, a parameter of parasympathetic activity, after ingestion was significantly higher in the C group than in the T group (p<0.05). No changes in LF power or LF/HF ratio, parameters of sympathetic activity, were induced by ingestion in either the C or T groups. The parasympathetic nerve dominantly controls gastric motor function, but autonomic nervous activity is reduced in patients who are unable to masticate and swallow food, resulting in adverse effects on gastric motor function and excretion function. Mastication and swallowing not only prepare food for passage from the oral cavity to the esophagus but are also important in terms of subsequent events that occur in stomach. It has been proposed that autonomic nervous activity might be involved in mastication and swallowing.

Effects of posture on the physiology of gastric emptying: A magnetic resonance imaging study

Objective. Gastric contents empty from the stomach despite frequent changes in body position. The mechanism that maintains gastric emptying independent of position is poorly understood. The aim of this study was to determine the effects of body position on gastric emptying and motor function. Material and methods. Twelve volunteers were investigated in seated position (SP) and upside-down position (UDP) after ingestion of 300 ml water. Magnetic resonance imaging provided a non-invasive assessment of gastric emptying and volumes, intragastric distribution and peristaltic function. Results. A marked difference in distal/proximal intragastric distribution between UDP and SP was present (7% versus 40%; p < 0.01). Gastric-emptying time was similar but emptying pattern was linear in UDP and exponential in SP. Peristalsis was slower in UDP than SP (2.75 versus 2.96 min−1; p < 0.01), but no correlation was found between peristaltic frequency and the rate of gastric emptying in either position. Postprandial volume response (gastric relaxation) was greater in UDP than SP (280 versus 250 ml; p < 0.05). A correlation was found between gastric relaxation and gastric-emptying time in SP (r2=0.46) but not in UDP. Conclusions. The stomach maintains the rate of gastric emptying despite radical changes in body position and intragastric distribution of gastric contents. In SP, hydrostatic pressure (modulated by gastric tone) dictates the gastric emptying. In UDP, gastric emptying also appears to be mediated by continuous adaptation of gastric tone. These findings provide support for the hypothesis that the mechanism of gastric emptying resembles a “pressure pump” rather than a “peristaltic pump”.

Impaired gastric motility and its relationship to gastrointestinal symptoms in patients with chronic renal failure

Gastrointestinal (GI) symptoms are common in patients with chronic renal failure (CRF), but the pathogenesis of these symptoms is unclear. Gastric motor function in CRF patients remains controversial, and the correlation between GI symptoms and gastric motility is also unclear. The aim of this study was to elucidate the relationship between gastric motility and GI symptoms in patients with CRF. Gastric motility was evaluated with cutaneously recorded electrogastrographs (EGGs) and gastric emptying of a solid meal, using 13C-octanoic acid breath testing, in 21 patients with predialysis endstage CRF and in 21 matched healthy controls. GI symptom severity was quantified in all patients. The CRF patients had a significantly lower incidence of normogastria postprandially and a lower power ratio than did healthy controls on the EGGs, with the CRF patients showing delayed gastric emptying. Three patients with normal gastric motility had no GI symptoms, and ten patients with both abnormal EGG and delayed gastric emptying had significantly higher GI symptom scores than the patients without abnormalities. The patients with CRF showed gastric hypomotility, including impaired gastric myoelectrical activity and delayed gastric emptying. Gastric hypomotility appears to be an important factor in the generation of GI symptoms in patients with CRF.

Gastric motor and sensory function

Abnormalities of gastric sensory and motor function are considered key players in the pathogenesis of upper gastrointestinal symptoms in functional dyspepsia and in gastroparesis. This review summarizes recent progress in our understanding of normal and pathologic gastric sensory and motor function. Several novel tests have been developed to study gastric sensitivity and meal-induced accommodation, including scintigraphic analysis of meal distribution within the stomach, single photon emission computed tomography of gastric volumes, and nutrient or water challenge tests. Several studies have reported on the occurrence of delayed gastric emptying in functional dyspepsia and in gastroparesis, but the correlation with symptoms was generally poor. The pathways and neurotransmitter involved in gastric hypersensitivity are progressively being unraveled. Several studies have confirmed and focused on increased symptom occurrence after nutrient challenge in functional dyspepsia. The role of the proximal stomach in the control of food intake and the stomach as a target in the treatment of obesity are areas of intense research. Studies have reported on pharmacologic approaches as well as electric stimulation in the treatment of gastric sensorimotor dysfunction. Progress in our understanding of normal and abnormal gastric sensory and motor function may lead to new or improved treatment modalities. Areas of major advances are the study of meal-induced symptoms in functional dyspepsia, unraveling of the role of the stomach in the control of food intake, and the use of gastric electric stimulation in gastroparesis and in obesity.

Pathogenesis and therapy for idiopathic dyspepsia

Functional dyspepsia (FD) is one of the most common gastrointestinal disorders. This review summarizes recent progress in our understanding of the pathogenesis and therapy for FD. Although distinction among FD, irritable bowel syndrome, and reflux disease is difficult in population-based studies, separate entities can be recognized in patients who seek medical attention. The pathogenesis of FD remains unclear, but recent studies have demonstrated a role for acute gastrointestinal infection in triggering FD and in genetic polymorphisms of G-proteins in predisposing to FD. The role of abnormalities in gastric motor function, visceral hypersensitivity, and psychosocial factors in the pathophysiology of dyspeptic symptoms has been the topic of multiple studies. Treatment options for FD remain limited. Recent studies have focused on acid-suppressive drugs and on novel prokinetics. Progress in our understanding of the pathogenesis and pathophysiology of FD may lead to new or improved treatment modalities. Areas of major advances are the role of infection and genetic predisposition and studies on the role of abnormalities in gastric motility and sensitivity.

Effect of Gastric Volume or Emptying on Meal-Related Symptoms After Liquid Nutrients in Obesity: A Pharmacologic Study

Altered postprandial satiation influences food intake in obesity. The aim of this study was to evaluate the contribution of gastric motor functions to intra- and postprandial symptoms in obese, otherwise healthy, people. In a randomized, parallel-group, double-blind design, 40 obese (body mass index>30 kg/m2) healthy volunteers (n=10/group) received intravenous saline (placebo), atropine (.02 mg/kg), or erythromycin (1 or 3 mg/kg) to alter gastric volume and emptying after liquid nutrient meals, measured by validated imaging methods. The nutrient drink test assessed the volume ingested at maximum satiation, and intra- and early postprandial symptoms. Relationships between gastric motor functions, meal size, and symptoms were assessed by using multiple regression. Circulating levels of candidate upper-gut hormones involved in satiation were measured. Relative to placebo, atropine retarded gastric emptying and increased gastric volumes; erythromycin accelerated gastric emptying and reduced gastric volumes during fasting. Although similar maximal tolerated volumes were recorded across treatments, intra- and immediate postprandial symptoms were increased by these perturbations, particularly nausea and bloating. Upper-gut hormonal profiles generally reflected changes in gastric emptying. Regression analysis showed that fasting predrug gastric volume was a significant predictor of intra- and postprandial bloating. Change in gastric volume postdrug or postmeal did not contribute additionally to predicting intra- or postprandial symptoms. There was significant (negative) association between gastric emptying and fullness score, and significant (positive) association with hunger score 30 minutes postprandially. In obese individuals, fasting gastric volumes and gastric emptying, but not postprandial gastric volumes, were associated with intra- and postprandial symptoms. Understanding the determinants of gastric volume may provide insights on mechanisms controlling satiation.

Insulin-Induced Hypoglycemia Stimulates Gastric Vagal Activity and Motor Function without Increasing Cardiac Vagal Activity

Background/Aims: We investigated whether increasing the efferent vagal activity by insulin-induced hypoglycemia would enhance gastric emptying and volumes in healthy subjects. Methods: Twenty healthy volunteers (10 males) were examined with and without vagal stimulation by insulin-induced hypoglycemia using a glucose clamp technique. Stomach function was tested by drinking meat soup (0.04 kcal ml^–1) at a rate of 100 ml min^–1 until maximal capacity. Intragastric volume at maximal drinking capacity was determined by three-dimensional ultrasound. Respiratory sinus arrhythmia (RSA) was used as an index of cardiac vagal activity and plasma pancreatic polypeptide (PP) as a measure of gastric vagal activity, and skin conductance (SC) as a measure of sympathetic tone. Results: Insulin-induced hypoglycaemia increased drinking capacity (p = 0.002), gastric emptying (p = 0.02), PP (p = 0.004) and SC (p = 0.004), while intragastric volume was unchanged (p = 0.7) and RSA decreased (p = 0.03). Conclusion: Enhancement of gastric vagal activity by insulin-induced hypoglycemia increased drinking capacity and gastric emptying similarly, resulting in an unchanged intragastric volume. Enhanced efferent vagal activity to the stomach (as measured by PP) was not associated by enhanced cardiac vagal activity (as measured by RSA), possibly a consequence of stress-induced sympathetic activation during the procedure.

Effect of peripherally administered ghrelin on gastric emptying and acid secretion in the rat

Ghrelin is a gut peptide that is secreted from the stomach and stimulates food intake. There are ghrelin receptors throughout the gut and intracerebroventricular ghrelin has been shown to increase gastric acid secretion. The aim of the present study was to examine the effects of peripherally administered ghrelin on gastric emptying of a non-nutrient and nutrient liquid, as well as, basal and pentagastrin-stimulated gastric acid secretion in awake rats. In addition, gastric contractility was studied in vitro. Rats equipped with a gastric fistula were subjected to an intravenous infusion of ghrelin (10–500 pmol kg − 1 min − 1 ) during saline or pentagastrin (90 pmol kg − 1 min − 1 ) infusion. After administration of polyethylene glycol (PEG) 4000 with 51Cr as radioactive marker, or a liquid nutrient with 51Cr, gastric retention was measured after a 20-min infusion of ghrelin (500 pmol kg − 1 min − 1 ). In vitro isometric contractions of segments of rat gastric fundus were studied (10 − 9 to 10 − 6 M). Ghrelin had no effect on basal acid secretion, but at 500 pmol kg − 1 min − 1 ghrelin significantly decreased pentagastrin-stimulated acid secretion. Ghrelin had no effect on gastric emptying of the nutrient liquid, but significantly increased gastric emptying of the non-nutrient liquid. Ghrelin contracted fundus muscle strips dose-dependently (pD 2 of 6.93 ± 0.7). Ghrelin IV decreased plasma orexin A concentrations and increased plasma somatostatin concentrations. Plasma gastrin concentrations were unchanged during ghrelin infusion. Thus, ghrelin seems to not only effect food intake but also gastric motor and secretory function indicating a multifunctional role for ghrelin in energy homeostasis.

Transcriptional up-regulation of nNOS in the dorsal vagal complex during low endotoxemia

The present study analyses the expression and distribution of neuronal nitric oxide synthase (nNOS) in the brainstem of animals pre-treated with Escherichia coli or Helicobacter pylori LPS, at doses that modulate gastric motor function. Systemic administration of H. pylori LPS prevented in a dose-dependent manner (5, 40 and 100 μg kg − 1 , i.v.) the increase in intragastric pressure induced by 2-deoxy- d-glucose (200 mg kg − 1 , i.v.) in urethane-anaesthetized rats. Quantitative analysis showed a significant increase in the amount of nNOS mRNA induced by E. coli or H. pylori LPS (2 h later), in a segment of the brainstem containing the dorsal vagal complex (DVC). Immunohistochemical studies showed nNOS presence in the DVC of vehicle-treated rats. Both E. coli (40 μg kg − 1 , i.p.) and H. pylori LPS (100 μg kg − 1 , i.p.) significantly increased (2 h later) the number of nNOS immunoreactive cells in this area, mainly at the most rostral level. The present study shows that systemic administration of E. coli or H. pylori LPS induces a transcriptional up-regulation of the nNOS in the DVC of the brainstem and suggests a role for NO synthesis in this area in the control of gastric motor function under endotoxemia.

Gastric Motor and Sensory Functions in Obesity

In the vast majority of affected individuals, obesity involves overconsumption of food relative to calorie requirements. The sensory function of the stomach may play a key role in the cessation of food ingestion. This sensation of the stomach is, in part, determined by its motor functions, such as tone and compliance and the rate of emptying. However, studies of gastric emptying in normal-weight and obese persons have shown inconsistent results. Gastric capacity was larger in obese persons when tested with an intragastric latex balloon filled with water. In contrast, other studies using the barostat or imaging (single-photon emission computed tomography) techniques reported no differences in gastric volume or compliance between obese and lean subjects. On the other hand, increased body mass and fasting gastric volume are independently associated with delayed satiation under standard laboratory conditions of food ingestion. These data suggest that changes in gastric motor and sensory functions in obesity may present useful targets to prevent and treat obesity. Further well-controlled, validated studies are needed to clarify the potential role of altering the stomach's function as a means of controlling food intake in obesity.

Preoperative Glycemic Status Affects the Risk for Acid Aspiration Pneumonia in Elective Cesarean Delivery

Recent studies have emphasized the importance of serum glucose in the regulation of gastrointestinal function. Larger volume and more acidic gastric residue secondary to the delayed gastric emptying resulting from hormonal and mechanical factors and the high levels of placentally derived gastrin have been documented in late pregnancies. Pulmonary aspiration syndrome continues to be a major concern in obstetric anesthesia because the morbidity and mortality associated with this complication increase with the volume and acidity of the gastric aspirate. In contrast to the many studies about the effects of hypoglycemia or hyperglycemia on gastric acid secretion and motor function, no studies have been conducted to determine the effects of glycemic status on the gastrin release and actual preoperative gastric contents especially in pregnant women. The purpose of this study was to investigate the effects of prophylactic 5% dextrose infusion during overfasting period without inducing hyperglycemia on preoperative serum gastrin concentration, gastric pH and volume in pregnant women undergoing elective cesarean delivery.

Prolactin‐releasing peptide affects gastric motor function in rat by modulating synaptic transmission in the dorsal vagal complex

Prolactin-releasing peptide (PrRP) is a recently discovered neuropeptide implicated in the central control of feeding behaviour and autonomic homeostasis. PrRP-containing neurones and PrRP receptor mRNA are found in abundance in the caudal portion of the nucleus tractus solitarius (NTS), an area which together with the dorsal motor nucleus of the vagus (DMV) comprises an integrated structure, the dorsal vagal complex (DVC) that processes visceral afferent signals from and provides parasympathetic motor innervation to the gastrointestinal tract. In this study, microinjection experiments were conducted in vivo in combination with whole-cell recording from neurones in rat medullary slices to test the hypothesis that PrRP plays a role in the central control of gastric motor function, acting within the DVC to modulate the activity of preganglionic vagal motor neurones that supply the stomach. Microinjection of PrRP (0.2 pmol (20 nl)(-1)) into the DMV at the level of the area postrema (+0.2 to +0.6 mm from the calamus scriptorius, CS) markedly stimulated gastric contractions and increased intragastric pressure (IGP). Conversely, administration of peptide into the DMV at sites caudal to the obex (0.0 to -0.3 mm from the CS) decreased IGP and reduced phasic contractions. These effects occurred without change in mean arterial pressure and were abolished by ipsilateral vagotomy, indicating mediation via a vagal-dependent mechanism(s). The pattern of gastric motor responses evoked by PrRP mimicked that produced by administration of L-glutamate at the same sites, and both the effects of L-glutamate and PrRP were abolished following local administration of NMDA and non-NMDA-type glutamate receptor antagonists. On the other hand, microinjection of PrRP into the medial or comissural nucleus of the solitary tract (mNTS and comNTS, respectively) resulted in less robust changes in IGP in a smaller percentage of animals, accompanied by marked alterations in arterial pressure. Superfusion of brain slices with PrRP (100-300 nm) produced a small depolarization and increased spontaneous firing in 10 of 30 retrogradely labelled gastric-projecting DMV neurones. The excitatory effects were blocked by administration of TTX (2 mum) or specific glutamate receptor antagonists, indicating that they resulted from interactions of PrRP at a presynaptic site. Congruent with this, PrRP increased the amplitude of excitatory postsynaptic currents (EPSCs, 154 +/- 33%, 12 of 25 neurones) evoked by electrical stimulation in mNTS or comNTS. In addition, administration of PrRP decreased the paired-pulse ratio of EPSCs evoked by two identical stimuli delivered 100 ms apart (from 0.95 +/- 0.08 to 0.71 +/- 0.11, P < 0.05), whereas it did not affect the amplitude of inward currents evoked by exogenous application of L-glutamate to the slice. The frequency, but not amplitude of spontaneous EPSCs and action potential-independent miniature EPSCs was also increased by administration of PrRP, suggesting that the peptide was acting at least in part at receptors on presynaptic nerve terminals to enhance glutamatergic transmission. In recordings obtained from a separate group of slices, we did not observe any direct effects of PrRP on spontaneous discharge or postsynaptic excitability in either mNTS or comNTS neurones (n = 31). These data indicate that PrRP may act within the DVC to regulate gastric motor function by modulating the efficacy of conventional excitatory synaptic inputs from the NTS onto gastric-projecting vagal motor neurones.

Pediatric gastric and duodenal disorders

This review provides a summary of new developments regarding common diseases affecting the stomach and duodenum in children. Celiac disease seems to be more prevalent than previously thought in different areas of the world, including the United States. The value of different serologic screening tools and other noninvasive tests has been carefully assessed. HLA-DQ typing has been proposed as part of celiac disease screening testing for high-risk groups. The use of the newly defined pediatric Rome criteria is allowing recognition of nonulcer (or functional) dyspepsia as an entity that affects a sizable subset of children. Testing of gastric sensory and motor function is clarifying the pathophysiology of this condition in children and adolescents. Intriguing data are also emerging about the possible role of mucosal eosinophils and disaccharidase deficiencies in causing dyspeptic symptoms. Intrasphincteric injection of botulinum toxin A represents a novel technique to treat gastroparesis. In refractory cases, the use of a gastric electric stimulator has shown to be beneficial in idiopathic and diabetic gastroparesis. Progress has been made in understanding the epidemiology of Helicobacter pylori infection in developing countries and its role in causing a wide spectrum of symptoms in children. Several noninvasive methods for its diagnosis have been established. Recent developments in the diagnosis and management of gastric and duodenal pathologic conditions are making a significant impact on pediatric clinical care. Future studies will likely continue to explore the use of minimally invasive testing and interventions in such conditions.

American Gastroenterological Association medical position statement: Diagnosis and treatment of gastroparesis

This document presents the official recommendations of the American Gastroenterological Association (AGA) on Diagnosis and Treatment of Gastroparesis. It was approved by the Clinical Practice Committee on May 16, 2004, and by the AGA Governing Board on September 23, 2004.

A community-based, controlled study of the epidemiology and pathophysiology of dyspepsia

Dyspepsia is common in clinical practice and in the community. The relationship of the symptoms to meals and the pathophysiology in community dyspeptic patients is unclear. The purpose of this study was to measure symptoms, demographic features, and gastric motor and sensory functions associated with dyspepsia in the community. A Modified Bowel Disease Questionnaire was mailed to a random sample of Olmsted County, MN, residents. Dyspeptic patients and healthy controls identified among community respondents completed further questionnaires, Helicobacter pylori serology, gastric emptying by scintigraphy, gastric accommodation by 99mTc-single-photon emission computed tomography imaging, and postprandial symptoms and satiation by a nutrient drink test. A total of 34.1% of community respondents reported dyspepsia within the past year, frequent (at least 25% of the time in the past year) in 17.5%, and 18.4% reported meal-related dyspepsia. Dyspepsia was frequent and related to meals in 10.8% of respondents. Compared with nondyspeptic controls, community dyspepsia was associated with higher aggregate symptom scores and bloating after a fully satiating meal. Community dyspepsia also was associated with higher somatization scores (P = .001), reporting of other somatic symptoms (P = .07), and general severity score on the symptom checklist 90 (P = .01), but not with disordered motor or sensory function. Gastric volumes, gastric emptying, and maximum tolerated volumes were not significantly different between community controls and dyspeptic patients. Meal-related dyspepsia is an important component of dyspepsia in the community. Community dyspeptic patients have higher symptom scores after a fully satiating meal, consistent with gastric hypersensitivity. This is associated with higher somatization scores rather than disorders of gastric emptying or volumes.

Experimentally induced ulcers and gastric sensory-motor function in rats.

Prior studies have demonstrated that inflammation can sensitize visceral afferent neurons, contributing to the development of hyperalgesia. We hypothesized that both afferent and efferent pathways are affected, resulting in changes in motor and sensory function. Kissing ulcers (KU) were induced in the distal stomach by injecting 60% acetic acid for 45 s into a clamped area of the stomach. In controls, saline was injected into the stomach. A balloon catheter was surgically placed into the stomach, and electromyographic responses to gastric distension were recorded from the acromiotrapezius muscle at various times after ulcer induction. The accommodation reflex was assessed by slowly infusing saline into the distally occluded stomach. Gastric pressure changes in response to vagal stimulation were measured in anesthetized rats. Contractile function of circular muscle strips was examined in vitro using force-displacement transducers. KU caused gastric hypersensitivity that persisted for at least 14 days. Fluid distension of the stomach led to a rapid pressure increase in KU but not in control animals, consistent with an impaired accommodation reflex. Gastric ulcers enhanced the contractile response to vagal stimulation, whereas the effect of cholinergic stimulation on smooth muscle in vitro was not changed. These data suggest that inflammation directly alters gastric sensory and motor function. Increased activation of afferents will trigger vagovagal reflexes, thereby further changing motility and indirectly activating sensory neurons. Thus afferent and efferent pathways both contribute to the development of dyspeptic symptoms.