Dual effects of somatostatin analog octreotide on gastric emptying during and after intragastric fill.
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The effect of the somatostatin analog agonist octreotide (Oct) on gastric emptying of 12.5% glucose during and after intragastric fill was examined in nondeprived rats equipped with stainless steel gastric fistulas. The rate of intragastric infusion (1.0 ml/min) and the volumes delivered (6 or 12 ml) were within the ranges typically observed in rats normally ingesting the same stimulus. In experiment 1, a dose-related suppression of glucose emptying during 12-min infusions was obtained in response to Oct (0, 0.0014, 0.014, 0.14, and 1.4 nmol/kg sc) injected 60 min before the test. The highest dose tested yielded a 37% suppression of glucose solute emptying during fill. In experiment 2, the suppression of emptying during fill induced by Oct (1.4 nmol/kg) was reversed by 10 or 40 microgram/kg of the somatostatin antagonist cyclo(7-aminoheptanoyl-Phe-D-Trp-Lys-Thr[Bzl]). The antagonist did not by itself affect emptying. Experiment 3 showed that the suppression of emptying obtained with 0.14 and 1.4 nmol/kg Oct had disappeared when the gastric sample was withdrawn 36 min after the termination of 12-min glucose infusions. Experiment 4 showed that the Oct-induced reductions in emptying during 6- and 12-min infusions, in fact, were reversed within 6 min after infusion offset. The point of transition between suppressed and increased emptying did not depend on time from injection or from infusion onset but was linked to the offset of the intragastric infusion regardless of its duration. The present findings support the notion that separable mechanisms govern gastric emptying during vs. after gastric fill. (+info)
The effect of helicobacter pylori eradication therapy on gastric antral myoelectrical activity and gastric emptying in patients with non-ulcer dyspepsia.
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BACKGROUND: Dysmotility of the gastroduodenal region and delayed gastric emptying have been considered to play roles in non-ulcer dyspepsia. In addition, it has been reported that Helicobacter pylori induced inflammation of the gastric mucosa may affect gastric motility. AIM: To evaluate the effects of H. pylori eradication therapy on gastrointestinal motility and symptoms in non-ulcer dyspepsia patients. METHODS: A total of 46 non-ulcer dyspepsia patients were examined for gastric emptying, antral myoelectrical activity, H. pylori infection, and symptom scores. In H. pylori-positive non-ulcer dyspepsia patients, gastric emptying, antral myoelectrical activity, and symptom scores were also analysed 2 months after being cured of H. pylori infection. RESULTS: A total of 67.4% of the non-ulcer dyspepsia patients were H. pylori-positive. Both abnormal gastric emptying and antral myoelectrical activity were observed in non-ulcer dyspepsia patients. H. pylori-positive non-ulcer dyspepsia patients were divided into three groups according to their gastric emptying: the delayed gastric emptying group, the normal gastric emptying group, and the rapid gastric emptying group. In the delayed and rapid gastric emptying groups, the gastric emptying and symptom scores were improved significantly by the eradication therapy. However, there was no improvement in symptom scores in the normal gastric emptying non-ulcer dyspepsia group by the eradication therapy. CONCLUSIONS: Disturbed gastric emptying and antral myoelectrical activity play roles in non-ulcer dyspepsia. Helicobacter pylori infection, inducing disturbed gastric emptying, may cause some non-ulcer dyspepsia symptoms. Gastric emptying and symptom scores are improved by H. pylori eradication therapy in non-ulcer dyspepsia patients with disturbed gastric emptying. H. pylori eradication therapy is effective in H. pylori-positive non-ulcer dyspepsia patients with disturbed gastric emptying. (+info)
Endogenous nitric oxide in the regulation of gastric secretory and motor activity in humans.
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BACKGROUND: Studies in animals have shown that nitric oxide (NO) affects gastric secretory and motor functions. However, little information is available about the involvement of this substance in the control of gastric secretory and motor activity in man. METHODS: This study, performed on 18 healthy, Helicobacter pylori-negative volunteers, was designed to evaluate the role of NO in the control of gastric acid secretion and of gastrin and somatostatin release in response to ordinary feeding (group A) and on gastric motor and electrical activity (group B). Gastric acid secretion was determined by means of intragastric pH-metry before and after feeding with a semi-liquid meal. Plasma levels of gastrin and somatostatin were measured using specific radioimmunoassays. Gastric emptying rate was measured using the 13C-acetate breath test, antral motor activity using a manometric catheter and myoelectric activity using cutaneous electrogastrography. Studies were repeated following pre-treatment with NG-monomethyl-L-Arginine (L-NMMA), L-Arginine (L-Arg) or their combination. RESULTS: L-NMMA delayed the recovery of intragastric pH to the pre-meal value, and suppressed postprandial gastrin release while increasing the plasma somatostatin level. L-Arg did not affect postprandial pH and plasma hormones, but reversed L-NMMA-induced alterations in intragastric pH and in plasma gastrin and somatostatin levels. Both postprandial antral motor activity (motility index) and gastric emptying significantly increased in tests with L-NMMA, but this was not observed when L-NMMA was given in combination with L-Arg or when L-Arg alone was used. The gastric electrical pattern, as measured by cutaneous electrogastrography, was not affected by L-NMMA, L-Arg or their combination. CONCLUSIONS: (1) Endogenous NO appears to be involved in the regulation of postprandial gastric acid secretion. This effect may be mediated by the changes in release of gastrin and somatostatin. (2) Endogenous NO delays gastric emptying and antral motor activity without affecting gastric myoelectrical activity. (+info)
Impact of gastric emptying on the pharmacokinetics of ethanol as influenced by cisapride.
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AIMS: To examine the influence of cisapride on the pharmacokinetics of ethanol and the impact of gastric emptying monitored by the paracetamol absorption test. METHODS: Ten healthy male volunteers took part in a cross-over design experiment. They drank a moderate dose of ethanol 0.30 g kg-1 body weight exactly 1 h after eating breakfast either without any prior drug treatment or after taking cisapride (10 mg three times daily) for 4 consecutive days. In a separate study, the same dose of ethanol was ingested on an empty stomach (overnight fast). Paracetamol (1.5 g) was administered before consumption of ethanol to monitor gastric emptying. Venous blood was obtained at 5-10 min intervals for determination of ethanol by headspace gas chromatography and paracetamol was analysed in serum by high performance liquid chromatography (h.p.l.c.). Results The maximum blood-ethanol concentration (Cmax ) increased from 3.8+/-1.7 to 5.6+/-2.3 mmol l-1 (+/-s.d.) after treatment with cisapride (95% confidence interval CI on mean difference 0.28-3.28 mmol l-1 ). The area under the blood-ethanol curve (AUC) increased from 6.3+/-3.5 to 7.9+/-2.6 mmol l-1 h after cisapride (95% CI -0. 74-3.9 mmol l-1 h). The mean blood ethanol curves in the cisapride and no-drug sessions converged at approximately 2 h after the start of drinking. Both Cmax and AUC were highest when the ethanol was ingested on an empty stomach (Cmax 9.5+/-1.7 mmol l-1 and AUC 14. 6+/-1.9 mmol l-1 h), compared with drinking 1 h after a meal and regardless of pretreatment with cisapride. CONCLUSIONS: A small but statistically significant increase in Cmax occurred after treatment with cisapride owing to faster gastric emptying rate as shown by the paracetamol absorption test. However, the rate of absorption of ethanol, as reflected in Cmax and AUC, was greatest after drinking the alcohol on an empty stomach. The cisapride-ethanol interaction probably lacks any clinical or forensic significance. (+info)
Influence of H. pylori infection on meal-stimulated gastric acid secretion and gastroesophageal acid reflux.
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Gastric acid secretion, gastrin release, gastric emptying, and gastroesophageal acid reflux were measured in asymptomatic individuals before and after elimination of Helicobacter pylori gastritis. After basal gastric acid secretion and serum gastrin concentrations were measured, meal-stimulated gastric acid secretion and gastrin release were assessed during in vivo intragastric titration to pH 3. Experiments were repeated 4 wk after treatment with lansoprazole, amoxicillin, and clarithromycin. Esophageal pH was also monitored for 24 h before and after therapy. Basal gastric acidity increased approximately 20 mmol/l in subjects whose infection was eradicated (P < 0.05) but not in those with persistent infection. Basal and meal-stimulated gastric acid secretion did not change after H. pylori eradication, despite a 41% reduction in meal-stimulated gastrin release (P < 0.05). Gastroesophageal acid reflux increased two- to threefold after successful treatment (P < 0. 05) but did not change in subjects with persistent infection. Thus elimination of H. pylori gastritis increases gastric acidity, probably by reducing nonparietal alkaline secretion, and this may facilitate gastroesophageal acid reflux. (+info)
Development of a test to measure gastric accommodation in humans.
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Postprandial symptoms of bloating, distension, early satiety, and nausea are associated with impaired postprandial gastric accommodation, which is detectable by means of an intragastric, barostatically controlled balloon in the proximal stomach and by ultrasound in the distal stomach. Our aim was to develop a noninvasive method to measure the entire gastric accommodation reflex. In 10 healthy volunteers, we used single photon emission computed tomography (SPECT) to measure fasting and postprandial gastric volumes. This method involved intravenous injection of (99m)Tc pertechnetate and gastric reconstruction of tomographic images with Analyze software. SPECT-Analyze imaging detects the postprandial gastric accommodation reflex in vivo. Mean fasting gastric volume was 182 +/- 11 (SE) ml and mean postprandial volume was 690 +/- 32 ml (P < 0.001). Both proximal and distal segments of stomach showed a two- to almost fourfold difference in volumes postprandially. Intraobserver coefficients of variation in estimated fasting and postprandial volumes were 9 and 8%; interobserver variations were 13 and 12%, respectively. SPECT-Analyze noninvasively measures postprandial gastric (total, proximal, and distal) accommodation in humans. This method appears promising to compare the accommodation response in health and disease and to perform mechanistic studies of the accommodation response. (+info)
Psychological and sex features of delayed gut transit in functional gastrointestinal disorders.
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BACKGROUND: The relation of demographic and psychological factors to the presence and extent of gut transit impairment in the functional gastrointestinal disorders has received little attention. AIMS: To compare the psychosocial and demographic features of patients with functional gastrointestinal disorders and delayed transit in one region of the gastrointestinal tract with those displaying more widespread delayed transit (that is, delay in two or three regions), and those with normal transit in all three regions. PATIENTS: Of 110 outpatient participants who satisfied standardised criteria for functional gastrointestinal disorders, 46 had delayed transit in one region, 32 had delay in two or three regions, and 17 exhibited normal transit in all regions. METHODS: Transit in the stomach, the small intestine, and the large intestine was assessed concurrently using a wholly scintigraphic technique; psychological status was assessed using established psychometric measures. RESULTS: Patients with delayed transit displayed demographic and psychological features that contrasted with patients with normal transit in all regions. In particular, widespread delayed transit featured female sex, a highly depressed mood state, increased age, frequent control of anger, and more severe gastric stasis, while the features distinguishing normal transit were male sex and high levels of hypochondriasis. CONCLUSION: These data suggest the existence of a distinct psychophysiological subgroup, defined by the presence of delayed transit, in patients with functional gastrointestinal disorders. (+info)
Gastric response to increased meal viscosity assessed by echo-planar magnetic resonance imaging in humans.
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Normal meals are highly viscous, and viscosity is a key factor in influencing gastric emptying of food. However, the process of meal dilution and mixing is difficult to assess with the use of conventional methods. The aim of this study was to validate an in vivo, novel, noninvasive, echo-planar magnetic resonance imaging (EPI) technique, capable of monitoring the viscosity of a model meal, and to use this to investigate the effects of viscosity on gastric emptying, meal dilution and satiety. Healthy volunteers (n = 8) ingested 500 mL of locust bean gum (0.25, 0.5, 1.0 or 1.5 g/100 g), nonnutrient, liquid meals of varying viscosities, and labeled with a nonabsorbable marker, phenol red. Meal viscosity was calibrated against the water proton transverse relaxation rate (T(2)(-1)) in vitro before ingestion, thus viscosity was measured in vivo via EPI measurements of T(2)(-1). Viscosity and dilution were also measured directly using nasogastric aspirates. Gastric volumes as measured by EPI, fullness, appetite and hunger were also assessed serially. Before ingestion, the log of initial meal viscosity was linearly related to T(2)(-1) (n = 8, r(2) = 0.95). Similarly, T(2)(-1) measured in vivo was also linearly related to the viscosity of the aspirates (r(2) = 0.88). All meals underwent rapid dilution, leading to a reduction in viscosity, which was greatest for the most viscous meal (P < 0.01). Surprisingly, despite the fact that the initial meal viscosity varied 1000-fold, there was only a small delay in gastric emptying (P for trend < 0.05). The area under the curve for satiety increased with initial meal viscosity, whereas that for hunger decreased (P < 0.05). In conclusion, the viscosity of a meal in vivo can be measured noninvasively using EPI. The stomach responds to meal ingestion by rapid intragastric dilution, causing a reduction of meal viscosity, and gastric emptying is minimally delayed. However, increased viscosity is associated with more prolonged satiety. (+info)