Secretin is an enterogastrone in humans

We studied in humans the effect of exogenous secretin in a physiological dose on gastric acid secretion stimulated by pentagastrin and postprandial plasma gastrin concentration. Two doses of pentagastrin, 80 and 160 pmol/kg/hr were used to stimulate gastric acid secretion. Secretin in two doses, 2.8 and 5.6 pmol/kg/hr were tried to study the response on stimulated gastric acid secretion. Intravenous secretin in a dose of 5.6 pmol/kg/hr significantly inhibited the gastric acid output stimulated by intravenous pentagastrin in a dose of 160 pmol/kg/hr, from 11.25±1.5 to 5.99±1.34 meq/hr, while lower dose of intravenous secretin (2.8 pmol/kg/hr) failed to inhibit the gastric acid output stimulated by the same dose of pentagastrin. However, the lower dose of intravenous secretin (2.8 pmol/kg/hr) inhibited the gastric acid output significantly from 8.78±1.21 to 6.37±1.62 meq/hr when gastric secretion was stimulated by the lower dose of pentagastrin (80 pmol/kg/hr). The plasma concentrations of secretin during intravenous secretin in a dose of 2.8 pmol/kg/hr was similar to postprandial plasma concentrations of secretin as previously reported. Doubling the dose of intravenous secretin resulted in almost twofold higher plasma concentrations than postprandial plasma concentrations. In addition, the low dose of secretin (2.8 pmol/kg/hr) suppressed the integrated postprandial gastrin response from 13.9±3.7 to 11.2±2.8 ng/min/ml (P=0.05) when endogenous release of secretin was blocked by intravenous cimetidine. Since the dose of pentagastrin and secretin employed in this study fell in a physiologic range, the inhibitory effect of secretin on stimulated gastric acid secretion appears to be a physiologic action in humans. Contrary to the findings in dogs, the inhibitory action of secretin on gastrin release was not statistically significant but was highly suggestive.     

The effects of rabeprazole on parietal cells and enterochromaffin-like cells in rats: a comparison with omeprazole

Background. We investigated the effects of rabe-prazole compared with those of omeprazole on enterochromaffin-like cells and parietal cells in rats. Methods. Rabeprazole or omeprazole was administered for 7 days by intraperitoneal injection (100 mg/kg or 20 mg/kg once a day) and the serum gastrin concentration, the antral density of G cells and D cells, fundic histamine content, fundic H⁺, K⁺-ATPase mRNA level, and parietal cell morphology were determined. Results. Both rabeprazole and omeprazole inhibited gastric acid secretion and increased the intragastric pH to over 6.5, as well as causing a marked increase in the serum gastrin concentration. The serum gastrin level was lower with rabeprazole treatment than with omeprazole treatment at both doses. Also, the antral G-cell density was higher with omeprazole than with rabeprazole, while the increase in both the histamine content and the H⁺, K⁺-ATPase mRNA level in the fundic mucosa was higher with omeprazole treatment at both doses, with the difference being significant at 100 mg/kg. Ultrastructural examination indicated that the stimulation of parietal cells by omeprazole was stronger than that by rabeprazole. Conclusions. Rabeprazole treatment does not drive enterochromaffin-like cells and parietal cells as strongly as omeprazole treatment despite its potent acid suppressive effect, suggesting that it represents a new generation of proton pump inhibitors. Received: March 16, 2001 / Accepted: August 10, 2001     

Effect of glucagon on vagally induced gastric acid secretion in humans

The effect of a physiologically relevant dose of pancreatic glucagon, 85 pmol/kg/hr, or saline on gastric acid secretion induced by modified sham feeding (chew and spit), was studied in 10 healthy volunteers. Gastric pH was held constant (pH 5.5) by intragastric titration. Glucagon infusion inhibited gastric acid secretion significantly, from 19.6±1.5 mmol H⁺ per hour during saline, to 10.4±1.4 mmol H⁺ per hour. Blood glucose increased during glucagon infusion and remained constant during saline infusion. Serum gastrin concentrations increased significantly by sham feeding, during saline as well as glucagon infusion, and no difference between the gastrin response during saline or glucagon infusion was found. Thus glucagon, in a physiologic dose, reduces vagally mediated acid secretion by a gastrin-independent mechanism.This study was supported by the Danish Hospital Foundation for Medical Research, Region of Copenhagen, The Faroe Islands and Greenland.     

Gastric ulcer

In 15 patients with uncomplicated benign gastric ulcers, basal and peak gastric acid outputs and fasting serum gastrin levels were studied before and after healing. The mean basal acid output [4.0±1.3 (sem) mEq H⁺/hr], the mean peak acid output (29.5±5.1 mEq H⁺/hr), and the mean fasting serum gastrin level (80.3±16.7 pg/ml) in these patients did not change significantly with healing. Failure of gastric secretory function to change with healing suggests that mucosal resistance factors are more important than gastric acid secretion in the pathogenesis of a gastric ulcer.     

Effect of erythromycin on antroduodenal motility in children with chronic functional gastrointestinal symptoms

To evaluate the effects of erythromycin on antroduodenal motility in children with chronic functional gastrointestinal symptoms, we studied 35 consecutive subjects referred for diagnostic motility studies. We recorded fasting motility for >4 hr, then infused in random order either 1 or 3 mg/kg erythromycin intravenously over 1 hr and continued the study for another hour. Erythromycin induced phase III in 18 of 20 children who had phase III during fasting compared to only one of 15 who did not (P<0.001). The antral motility index increased after erythromycin (1596±323 vs 436±242 mm Hg/30 min before erythromycin,P<0.005) but the duodenal motility index did not change. The antral motility index was greater in children receiving 3 mg/kg than in those receiving 1 mg/kg (1968±391 vs 1226±285 mm Hg/30 min,P<0.01), but duodenal motility indices did not differ. Only one child receiving the lower dose erythromycin complained of abdominal pain, nausea, or vomiting vs 9 of 19 the children receiving the higher dose (P<0.02). In summary, in children with chronic functional gastrointestinal disorders, erythromycin rarely induced phase III in patients who did not have it during fasting. When different doses erythromycin are compared, 1 and 3 mg/kg are equally efficacious in inducing phase III episodes; the lower dose is associated with fewer side effects and the higher dose produces a higher antral motility index.     

Gastric acid secretion and gastrin release in the baboon

Significant species differences have been demonstrated in gastric physiology, a factor that limits extrapolation of animal data to man. Primate physiology is thought to be similar to that of man; however, gastric function has not been adequately documented in the primate. In the present study six baboons (body weight 25.5±1.8 kg) were trained to sit in a chair and gastric acid secretion and gastrin release was studied in conscious animals. Mean basal acid secretion was 1.3±0.1 mmol (H⁺)/hr. Maximum output after pentagastrin (12 g/kg/hr) was 9.5±0.9 mmol (H⁺)/hr and 11.0±0.4 mmol (H⁺)/hr after histamine (40 g/kg/hr). A statistically significant (by cosinor analysis) circadian rhythm was demonstrated for intragastric pH over 24 hr in fasted baboons (P<0.001). Mean basal serum gastrin level was 37.7±8.3 pg/ml. The integrated gastrin response after administration of a protein rich meal was 2.52±0.07 ng×min/ml and this increased to 5.17±0.18 ng×min/ml (P<0.05) following simultaneous administration of a meal with atropine (0.2 mg/kg) (P<0.05). Our results suggest that there is significant basal and stimulated acid secretion in the baboon; the amount of acid secreted is similar to that reported in man. Gastric pH demonstrated a circadian rhythm. Postprandial gastrin release was significantly enhanced by cotreatment with atropine. As the present findings are similar to those previously reported in man, the baboon may be a useful model for further studies in gastric physiology and experimental peptic ulceration.     

Endogenous glucagon-like peptide 1 controls endocrine pancreatic secretion and antro-pyloro-duodenal motility in humans

BACKGROUND: Exogenous use of the intestinal hormone glucagon-like peptide 1 (GLP-1) lowers glycaemia by stimulation of insulin, inhibition of glucagon, and delay of gastric emptying. AIMS: To assess the effects of endogenous GLP-1 on endocrine pancreatic secretion and antro-pyloro-duodenal motility by utilising the GLP-1 receptor antagonist exendin(9-39)amide (ex(9-39)NH2). METHODS: Nine healthy volunteers underwent four experiments each. In two experiments with and without intravenous infusion of ex(9-39)NH2 300 pmol/kg/min, a fasting period was followed by intraduodenal glucose perfusion at 1 and 2.5 kcal/min, with the higher dose stimulating GLP-1 release. Antro-pyloro-duodenal motility was measured by perfusion manometry. To calculate the incretin effect (that is, the proportion of plasma insulin stimulated by intestinal hormones) the glycaemia observed during the luminal glucose experiments was mimicked using intravenous glucose in two further experiments. RESULTS: Ex(9-39)NH2 significantly increased glycaemia during fasting and duodenal glucose. It diminished plasma insulin during duodenal glucose and significantly reduced the incretin effect by approximately 50%. Ex(9-39)NH2 raised plasma glucagon during fasting and abolished the decrease in glucagon at the high duodenal glucose load. Ex(9-39)NH2 markedly stimulated antroduodenal contractility. At low duodenal glucose it reduced the stimulation of tonic and phasic pyloric motility. At the high duodenal glucose load it abolished pyloric stimulation. CONCLUSIONS: Endogenous GLP-1 stimulates postprandial insulin release. The pancreatic alpha cell is under the tonic inhibitory control of GLP-1 thereby suppressing postprandial glucagon. GLP-1 tonically inhibits antroduodenal motility and mediates the postprandial inhibition of antral and stimulation of pyloric motility. We therefore suggest GLP-1 as a true incretin hormone and enterogastrone in humans.     

Effect of gastric acid suppressants on human gastric motility

Background—The effect of histamine H₂receptor antagonists on gastric emptying is controversial.
Aims—To determine the effects of ranitidine,famotidine, and omeprazole on gastric motility and emptying.
Patients and methods—Fifteen normal subjectsunderwent simultaneous antroduodenal manometry, electrogastrography(EGG), and gastric emptying with dynamic antral scintigraphy (DAS).After 30 minutes of fasting manometry and EGG recording, subjectsreceived either intravenous saline, ranitidine, or famotidine, followed by another 30 minutes recording and then three hours of postprandial recording after ingestion of a radiolabelled meal. Images were obtainedevery 10-15 minutes for three hours to measure gastric emptying andassess antral contractility. Similar testing was performed afteromeprazole 20 mg daily for one week.
Results—Fasting antral phase III migrating motorcomplexes (MMCs) were more common after ranitidine (9/15 subjects,60%), famotidine (12/15, 80%), and omeprazole (8/12, 67%) comparedwith placebo (4/14, 29%; p<0.05). Postprandially, ranitidine,famotidine, and omeprazole slowed gastric emptying, increased theamplitude of DAS contractions, increased the EGG power, and increasedthe antral manometric motility index.
Conclusions—Suppression of gastric acid secretionwith therapeutic doses of gastric acid suppressants is associated withdelayed gastric emptying but increased antral motility.

Keywords:gastric motility; gastric emptying; histamineH₂ receptor antagonists; proton pump inhibitors; gastricacid secretion; scintigraphy

     

Effect of gastrin heptadecapeptide (G17) on oesophageal contractions in patients with diffuse oesophageal spasm.

An intravenous bolus of pentagastrin significantly increased the amplitude and duration of oesophageal body contractions in seven patients with diffuse oesophageal spasm (DES) when compared with five normal subjects (P greater than 0.05). In order to determine whether this stimulation also occurred at physiological gastrin concentrations, the effect of an intravenous infusion of gastrin heptadecapeptide (G17), 25 pmol/kg-h, on oesophageal contractions was studied in DES patients. G17 had no significant effect on the amplitude and duration of oesophageal contractions compared with a saline control. This dose of G17 was near the D50 for gastric acid secretion and produced a rise in serum gastrin concentration comparable with a meal. G17 infusions at doses of 100 and 200 pmol/kg-h increased the amplitude and duration of oesophageal contractions, but the corresponding serum gastrin concentrations were higher than postprandial levels. Thus, endogenous fluctuations in serum gastrin heptadecapeptide, alone, are unlikely to alter oesophageal contractions in DES patients.     

Cephalic stimulation of gastrointestinal secretory and motor responses in humans.

The present study was designed (a) to investigate the cephalic phase of gastropancreatic secretion, antroduodenal motility, and regulatory peptide release in six healthy young men and (b) to assess its regulation by the cholinergic system and endogenous cholecystokinin. Sham feeding performed for 15 minutes induced a concurrent stimulation of gastropancreatic secretion, antroduodenal motility, and pancreatic polypeptide release that lasted for 30 minutes. Reappearance of interdigestive phases III was retarded in the post-sham-fed state. Atropine abolished secretory, motor, and pancreatic polypeptide responses to sham feeding and enhanced gastrin release. The cholecystokinin receptor antagonist loxiglumide did not attenuate pancreatic enzyme response but diminished antral motor response by 72% (P less than 0.05) and release of pancreatic polypeptide by 91% (P less than 0.05); it enhanced gastrin release and abolished retardation of reappearance of phase III with sham feeding. It is concluded that (a) there is a distinct cephalic phase of gastropancreatic secretion, antroduodenal motility, and pancreatic polypeptide release in humans that is primarily under cholinergic control and that (b) endogenous cholecystokinin is involved in antral motor, gastrin, and pancreatic polypeptide responses to sham feeding.     

Effect of histamine H2-receptor stimulation on bombesin-and peptone-stimulated gastrin release in man

This study was undertaken to determine whether histamine H₂-receptors are involved in the regulation of gastrin secretion in man. Since previous studies on the effect of histamine H₂-receptor blockade on gastrin release are conflicting, we have studied the effect of histamine infusion (130 nmol/kg/hr) with simultaneous H₁-receptor blockade on gastrin release in healthy male subjects. Intragastric pH was maintained at 4.5 by continuous intragastric titration during all studies. Histamine did not affect gastrin release stimulated by infusion of bombesin (90 pmol/kg/hr) or by a peptone meal. Integrated gastrin secretion during bombesin plus histamine was 767±151 pmol·min/liter (±SEM), compared to 757±144 pmol·min/liter during bombesin plus saline (not significant), whereas integrated meal-stimulated gastrin release was 1666±456 pmol·min/liter during histamine and 1856±492 pmol·min/liter during saline. It is concluded that histamine H₂-receptors do not seem to be involved in the regulation of gastrin secretion in man.Supported by a grant from the Jan Kornelis de Cock-Stichting     

Physiological role of cholecystokinin on gastric emptying and acid output in dogs

We investigated the physiological role of cholecystokinin (CCK) on gastric emptying and acid secretion in seven conscious dogs with gastric cannulae. Two hundred milliliters of a 4% amino acid meal was given via the cannula, and both gastric emptying and acid output were measured concurrently using a dye-dilution technique. Gastric emptying of the liquid amino acid meal was exponential, and the acid output and plasma concentrations of CCK, gastrin, and somatostatin peaked within 30 min after the meal. Intravenous infusion of CCK-8 at 28 and 56 pmol/kg/hr but not 14 pmol/kg/hr increased plasma levels of the peptide and inhibited gastric emptying as well as acid output. Plasma gastrin was not affected significantly by the CCK infusion, whereas plasma somatostatin increased significantly in response to 56 pmol/kg/hr of CCK-8. Loxiglumide, 22 µmol/kg/hr, significantly enhanced gastric emptying and augmented acid output, as well as plasma gastrin response, whereas it abolished the postprandial rise in plasma somatostain. We concluded that in dogs, CCK plays an important role in the physiologic regulation of postprandial gastric emptying of a liquid caloric meal and acid output. Its inhibitory effect on gastric acid secretion appears to be mediated, at least in part, by somatostatin.The opinions and assertions contained herein are the private ones of the authors and are not to be construed as official or reflecting the views of the Department of Defense or the Uniformed Services University of the Health Science.The experiments reported herein were conducted according to the principles set forth in the Guide for the Care and Use of Laboratory Animals, Institute of Laboratory Animal Resources, National Research Council, HHS/NIH, Publ. No. 85-23.     

Effect of low-dose exogenous secretin on pentagastrin- and meal-stimulated gastric acid secretion in humans

Intravenous infusion of secretin in a dose of 0.05 CU/kg/hr inhibited pentagastrin-stimulated (100 ng/kg/hr) acid secretion by 42% (P<0.05) abd meal-stimulated (10% peptone, pH 5.5) acid secretion by 33% (P<0.05) in 10 healthy subjects. Median serum gastrin concentration during peptone stimulation was reduced by 24% (P<0.05) during secretin infusion. Median plasma secretin concentrations were 6.0 and 5.2 pmol/liter, respectively. Since these secretin concentrations are of the same magnitude as those seen after duodenal acidification, it is concluded that secretin may participate in the physiological inhibition of gastric acid secretion.Supported by grant 12-4525, Danish Medical Research Council     

Cholinergic effects on human gastric motility

BACKGROUND: Cholinergic regulation of chronotropic (frequency) and inotropic (force) aspects of antral contractility and how these impact on gastric emptying are not well delineated. AIMS: To determine the effects of cholinergic stimulation and inhibition on myoelectric, contractile, and emptying parameters of gastric motility. METHODS: Ten normal subjects underwent three studies each, using simultaneous electrogastrography (EGG), antroduodenal manometry, and gastric emptying with dynamic antral scintigraphy (DAS). After 30 minutes of baseline fasting manometry and EGG, subjects received saline intravenously, atropine (0.6 mg then 0.25 mg/hour intravenously), or bethanechol (5 mg subcutaneously). This was followed by another 30 minutes' recording and by three hours of postprandial recording after ingestion of a technetium-99m labelled solid meal. RESULTS: During fasting, atropine decreased, whereas bethanechol increased, the antral manometric motility index and EGG power. Postprandially, atropine decreased the amplitude of antral contractions by DAS, decreased the postprandial antral manometric motility index, and slowed gastric emptying. Atropine caused a slight increase in postprandial frequency of antral contractions by DAS and gastric myoelectrical activity by EGG. Bethanechol slightly increased the amplitude, but slightly decreased the frequency of antral contractions by DAS and decreased the frequency of gastric myoelectrical activity by EGG, with no significant increase in the motility index or gastric emptying. CONCLUSIONS: Cholinergic antagonism with atropine reduces antral contractility and slows gastric emptying. Cholinergic stimulation with bethanechol increases antral contractility, but decreases the frequency of antral contractions, without altering the antral motility index or gastric emptying.     

Gastric Acid Inhibition by Antral Acidification Mediated by Endogenous Prostaglandins

The effects of indomethacin on the basal and stimulated gastric acid secretion at controlled intragastric pH were examined. Four tests with modified sham feeding were made in nine healthy volunteers on different occasions, twice with acid and twice with alkaline perfusion of the stomach. Blocking of the prostaglandin biosynthesis with indomethacin preceded one of the tests at each pH. Plasma levels of gastrin were measured. Antral acidification suppressed the basal and vagally stimulated gastric secretion rate of H⁺ and Cl^-. The inhibition was associated with a decreased plasma gastrin response. Indomethacin reduced the inhibition of the peak acid output and plasma gastrin levels induced by antral acidification. During alkalinization of the stomach indomethacin had no effect on the acid secretion rate or plasma gastrin levels. The results suggest that the pH-dependent inhibitory regulation of the gastric acid secretion is mediated by locally produced prostaglandins. The mechanism functions at least partially through modifying the release of gastrin.     

Effects of 13-nle-motilin on salivary,gastric, and pancreatic secretions in man

Salivary, gastric, and pancreatic secretory responses to intravenous 13-norleucine-motilin (13-nle-motilin), a synthetic analog of motilin and biologically equivalent to the natural polypeptide, were studied in healthy volunteers. 13-nle-Motilin in doses of 100 ng/kg body wt/hr significantly stimulated gastric pepsin output, while H⁺ secretion and serum gastrin levels remained unchanged. Enhanced pepsin secretion was not accompanied by an increase in gastric secretion of cyclic 3, 5-adenosine monophosphate, nor did gastric mucosal levels of the cyclic nucleotide rise. A dose of 13-nle-motilin, which stimulated gastric pepsin output, did not exert any significant effect on salivary and pancreatic secretions.     

Antral gastrin cells and serum gastrin in achlorhydria.

Forty-five patients with achlorhydria due to severe atrophic corpus gastritis or gastric atrophy were studied by determination of serum gastrin, histological examination of multiple biopsy from the antrum, and quantitation of gastrin cells revealed by an indirect immunofluorescence technique. In a reference group of 12 persons with normal gastric secretion and without atrophic antral gastritis the mean number of gastrin cells per field of vision was 52 +/- 6.5 (S.E.M.). In a group of achlorhydric patients having normal antral mucosa (n = 24), the serum gastrin levels was 324 +/- 56 pmol/l and the number of gastrin cells was 79.6 +/- 7.5 cells/field of vision. The corresponding values for a group of achlorhydric patients with chronic superficial antral gastritis (n = 11) were 361 +/- 186 pmol/l and 88.0 +/- 14.4 cells/field of vision. In a group of achlorhydric patients with atrophic antral gastritis (n = 10) serum gastrin was 15.0 +/- 3.3 pmol/l, and the number of gastrin cells was 6.2 +/- 3.3 cells/field of vision. Compared to the subjects in the reference group, the number of gastrin cells was significantly higher in the groups of achlorhydric patients with normal or superficially inflamed antral mucosa and significantly lower in achlorhydric patients with atrophic antral gastritis. It is concluded that serum gastrin in general is a good indicator for the presence or absence of antral atrophic gastritis in achlorhydria.     

An evaluation of an ambulatory manometry system in assessment of antroduodenal motor activity

While abnormalities in antroduodenal motor function have been documented in both organic and functional disorders, controversy surrounds the ideal manometric technique. We sought, therefore, to evaluate a digital solid-state ambulatory system. Sixteen normal volunteers underwent 24-hr recordings of antroduodenal motility. Following catheter placement, a standardized meal was ingested in the laboratory; thereafter, subjects were ambulatory and assumed normal diet and activities. The system was well tolerated; subjects reported that it did not affect their usual activities. Migrating motor complex (MMC) activity was identified in each subject (mean frequency: 4.1 MMCs/24 hr, range 1–8); on average 1.9 (range 0–4, frequency 0.1/hr) occurred while awake and 2.1 (range 0–5, 0.3/hr,P<0.05 vs awake) during sleep. The fed response was evaluated by calculating a motility index (MI) at 30-min intervals from 30 min before to 120 min following meal ingestion. Postprandially, MI was maximal during the first 30 min following meal ingestion: MI (mean±sd) 30 min before vs 30 min after meal in the antrum: 4.16±1.42 vs 5.33±0.72 (P<0.05), duodenum: 4.04±0.80 vs 4.57±0.47 (P<0.05), respectively. None of the other postprandial intervals were significantly different from baseline. There was no significant difference in MI between the standard andad libitum meals. Retrograde catheter migration (mean 5.6, range 1–10 cm) occurred in relation to all meals; as a consequence, antral recordings were lost following 60% of all meals, thereby limiting meaningful analysis of the antral fed response. We conclude, firstly, that while an ambulatory antroduodenal manometry system is well tolerated and reliably records duodenal motility, postprandial catheter migration limits antral recordings, and, secondly, that a motility index calculated during the first 30 min following anad libitum meal accurately reflects the fed motor response.Supported in part by the University of Nebraska Hospital.     

Importance of gastric motility in the pathogenesis of indomethacin-induced gastric lesions in rats

Effects of indomethacin on gastric motility and secretion, and levels of endogenous prostaglandins (PGs) were investigated in rats, in attempts to elucidate the factors involved in the pathogenesis of indomethacin-induced macroscopic gastric lesions. Subcutaneous administration of indomethacin had no effect on the gastric mucosa at doses of 1 and 5 mg/kg, but induced visible lesions dose dependently at over 10 mg/kg within 4 hr. At 25 mg/kg, there were apparent nonhemorrhagic lesions within 1 hr, and these lesions became hemorrhagic with time. Acid secretion was not affected by this agent at either dose level, but pepsin or acid-induced HCO₃ ^– secretion was significantly increased or decreased, respectively, at a dose less than 5 mg/kg, which did not induce any lesion. Gastric motility, however, was dose dependently increased after administration of indomethacin, and its effect was significant at 10 mg/kg or greater. Time-course changes in the motility were in parallel with those of the lesion formation. PGE₂ and 6-keto PGF₁ levels in the corpus mucosa were reduced around 80–90% for more than 4 hr from 30 min after administration of 5 mg/kg or more of indomethacin. When all the above changes caused by indomethacin were plotted for the various doses, a significant correlation (r=0.958, P<0.01) was found between the lesion index and the changes in motility, but not in other factors, including PG levels. These results indicate that gastric motility may be an important factor in the pathogenetic mechanism of indomethacin-induced gastric lesions in rats. A deficiency of endogenous PGs may be a prerequisite for later extension of the lesions.     

Gastroduodenal motility in chronic dyspepsia. 2. Postprandial motility

After ingestion of a solid test meal the postprandial motor activity in 17 dyspeptic patients and 12 healthy controls were examined. In all individuals the gastric emptying was measured by scintigraphy. - The antral pressure activity after food intake was delayed in dyspepsia and showed a distinct reduction with time (antral hypomotility). In contrast the postprandial duodenal motility was increased significantly (duodenal hyperdyskinesia). All 6 dyspeptic patients with prolonged gastric emptying had gastroduodenal manometric abnormalities. - Our results suggest that in chronic dyspepsia the interdigestive and postprandial motility is often disturbed. The delayed gastric emptying occurs because of impaired antral peristalsis and/or increase of duodenal resistance.