Consequences of antral and duodenal acidification on acid secretion, gastrin response and gastric emptying in duodenal ulcer patients and normal subjects

The present study intended to investigate the effect of antroduodenal acidification on gastric acid secretion and emptying, gastrin and somatostatin release in response to food in healthy subjects as well as in duodenal ulcer patients. Ten duodenal ulcer patients and 9 normal controls were studied twice: the same 400 ml liquid protein meal (proteins: 10 g) was introduced into the stomach; then intragastric pH was either maintained at pH 4.5 or allowed to decrease in response to the meal. Acid secretion was calculated using the intragastric titration method (for which the intragastric pH is fixed at pH 4.5) and using the serial dilution indicator method (which allows antral acidification) respectively. Gastric emptying was estimated according to: a) iterative measurements of intragastric meal residual volume; b) volume passing through the pylorus. These two tests were performed in a random order and during each, plasma gastrin and somatostatin responses to the meal were determined. In healthy subjects, antral acidification following the meal was associated with a significantly lower acid secretion (17.3 +/- 0.9 mmol/h; m +/- SEM) than when the pH was maintained at pH 4.5 (20.2 +/- 1.3; p less than 0.05). Moreover, gastric emptying was slower when the pH was allowed to decrease (t 1/2: 26.2 +/- 1.4 min) than when the pH was constant (t 1/2: 20.5 +/- 2.2 min; p less than 0.05). By contrast, in the duodenal ulcer group, neither acid output nor gastric emptying were significantly different in the two situations.(ABSTRACT TRUNCATED AT 250 WORDS)     

Gastric emptying of solids, acid secretion and tobacco in duodenal ulcer]

We study in a group of patients with endoscopically diagnosed duodenal ulcer (19; 17 males) and controls (11; 7 males) the gastric emptying of solids through scintigraphy and gastric acid secretion by standard tests. In the same way we investigated prospectively some clinical data, specially smoking habits. As a whole, patients with duodenal ulcer showed an emptying of solids slightly faster than controls (T 1/2-minutes-: 85.4 +/- 28.6 in patients with duodenal ulcer versus 116.9 +/- 46.5 in controls, p less than 0.03). However, most of our patients (15 of 19 or 79%) were found to have a normal emptying rate. No correlation was found between secretory outputs and gastric emptying. Smokers with duodenal ulcer had a faster emptying that non-smokers with duodenal ulcer (T 1/2 74.8 +/- 30.05 vs. 99.91 +/- 19.86; p = 0.05).     

Total 24-hour gastric acid secretion in patients with duodenal ulcer. Comparison with normal subjects and effects of cimetidine and parietal cell vagotomy

The purposes of these studies were as follows: (a) to compare gastric acid secretion throughout an entire 24-h period in 8 patients with duodenal ulcer disease and in 7 normal subjects, and (b) to determine in duodenal ulcer patients to what extent total, 24-h acid secretion was reduced by oral cimetidine (n = 7) or parietal cell vagotomy (n = 7). Basal, interprandial, and nocturnal acid secretion were measured by gastric aspiration, whereas acid secretion in response to breakfast, lunch, and dinner was measured by in vivo intragastric titration. Total, 24-h acid secretion averaged 408.3 +/- 61.7 mmol in duodenal ulcer patients and 208.3 +/- 18.5 mmol in normal subjects (p less than 0.02). Acid secretion was higher in duodenal ulcer patients than in normal subjects during both day (p less than 0.01) and night (p less than 0.05). Cimetidine (400 mg twice daily) significantly (p less than 0.001) reduced total, 24-h acid secretion in duodenal ulcer patients to 235.3 +/- 58.6 mmol, a rate that was not significantly different from 24-h acid secretion in normal subjects. On the other hand, total, 24-h acid secretion averaged only 86.7 +/- 20.7 mmol after parietal cell vagotomy, a rate that was significantly lower than 24-h acid secretion in normal subjects (p less than 0.001) and in duodenal ulcer patients receiving cimetidine (p less than 0.05). These studies indicate that patients with duodenal ulcer disease secrete excessive amounts of gastric acid during the day and night and throughout an entire 24-h period. A twice-daily 400-mg dose of cimetidine reduces 24-h acid secretion in duodenal ulcer patients to nearly normal rates, whereas parietal cell vagotomy reduces acid secretion to well below normal rates.     

Effect of graded amounts of acid instilled into the duodenum on pancreatic bicarbonate secretion and plasma secretin in duodenal ulcer patients and normal subjects.

Pancreatic bicarbonate secretion and plasma secretin were measured in response to graded amounts of hydrochloric acid (0.94, 1.88, 3.75, and 7.5 mEq per 5 min) instilled directly into the duodenum in duodenal ulcer patients and in normal subjects. These graded amounts of acid produced graded increases in pancreatic bicarbonate in both groups. Mean bicarbonate secretion was significantly greater in the duodenal ulcer patients than in the normal subjects basally and after the lowest dose of hydrochloric acid. Mean (+/- SE) peak 30-min bicarbonate output (in milliequivalents) after duodenal acidification was 3.0 +/- 1.0 in the duodenal ulcer patients and 2.1 +/- 0.6 in the normal subjects (P less than 0.5). A significant (P less than 0.05) increase in plasma secretin occurred after duodenal acidification, but the increase in the duodenal ulcer and normal subjects was not significantly different (P less than 0.2). These results indicate that pancreatic bicarbonate secretion and increase in plasma secretin in response to graded amounts of duodenal acid are at least as great in patients with duodenal ulcer as in normal subjects.     

Altered Concentrations of Gastrin-Releasing Polypeptide and Somatostatin in Fundic and Duodenal Bulb Mucosa of Patients with Duodenal Ulcer Disease

The concentrations of gastrin-releasing polypeptide, somatostatin (SS), and gastrin in extracts of endoscopically obtained biopsies from the fundus, antrum, and duodenum of patients with uncomplicated bile stones (controls) or duodenal ulcer disease were measured with specific radioimmunoassays. The validity of the tissue sampling was confirmed by characteristic and significant differences between gastrin concentrations at the different biopsy sites. Gastrin-releasing polypeptide levels were at their highest in the fundic and duodenal bulb compared to the antrum in controls (p less than 0.01), whereas no differences in gastrin-releasing polypeptide content of the different parts of the stomach were found in duodenal ulcer patients. Compared to controls gastrin-releasing polypeptide in duodenal ulcer patients was reduced in fundic and duodenal bulb mucosa (p less than 0.01). SS levels were highest (p less than 0.05) in the first part of duodenum in controls. Compared to controls duodenal ulcer patients had lower SS concentrations present in fundic (p less than 0.01) and highest SS concentrations present in duodenal bulb mucosa (p less than 0.01). There was no correlation between acid secretion and mucosal gastrin-releasing polypeptide or SS concentrations in any part of the stomach and duodenum.     

The effect of intragastric pH-variations on the gastric acid response to insulin hypoglycaemia in healthy subjects and duodenal ulcer patients.

The gastric acid response to i.v. injection of 0.15 U of soluble insulin/kg b.w. was determined in healthy subjects and duodenal ulcer patients during intragastric perfusion with water, 0.1 M HC1, and alkaline buffer (pH 8.3). Perfusion with hydrochloric acid significantly reduced the peak gastric acid output following insulin in 6 healthy subjects (reduction 45%, p less than 0.05) but had no significant effect on the peak gastric acid response to insulin in 7 DU patients (reduction 16%, p greater than 0.05). The 2.5-hour gastric acid response to insulin was, however, significantly reduced in both groups (56% and 35%, respectively) by exogenous acidification of the stomach. The gastric acid response to insulin hypoglycaemia in 3 DU patients was the same with intragastric water and alkaline buffer perfusion. The reduction of the gastric acid response to insulin hypoglycaemia by intragastric acidification corresponded to a reduced volume secretion and could not be ascribed to increased back diffusion of hydrogen ions or duodenal inhibition. These findings suggest that the gastric acid response to insulin hypoglycaemia is inhibited by a low intragastric pH in man, and that DU patients are less sensitive to the inhibitory mechanism than healthy subjects.     

A Double-Blind Randomized Study Comparing Different Dose Regimens of H2-Receptor Antagonists on 24-Hour Gastric Secretion in Normal Subjects and Duodenal Ulcer Patients

Duodenal ulcer therapy with H2 antagonists initially aimed to control acid secretion throughout the 24-h period, but recently nighttime suppression has been advocated. The effect of single nighttime regimens of cimetidine 400 mg BID, cimetidine 800 mg HS, ranitidine 150 mg HS, and placebo on 24-h intragastric acidity, nocturnal acid output, and pepsin secretion were studied in four healthy volunteers and four patients with healed duodenal ulcer. A nonrandomized dose of cimetidine 1200 mg HS was also studied. For all four treatments, daytime (0730-2230 h) intragastric acidity was reduced by 4-30% in the normals and by 10-44% in the duodenal ulcer patients (NS), while 24-h intragastric acidity was reduced by 44-46% and 40-64%, respectively (p less than 0.05). Reduction in nocturnal acid output was 82-96% in normals and 91-99% in duodenal ulcer, respectively. Pepsin concentration was unaffected by treatment but pepsin concentration was significantly (p less than 0.05) lower in patients than in normals. Mean 24-h gastric acid secretion was reduced by a single nighttime treatment with an H2-receptor antagonist, while nocturnal acid secretion was virtually abolished. H2 antagonists given only at night deserve further clinical evaluation to determine the minimal effective dose and optimal duration of suppression to achieve ulcer healing.     

Duodenal gastrin concentration in upper gastrointestinal disorders

Duodenal gastrin concentration was measured in endoscopic forceps biopsy specimens of the juxtapyloric duodenal mucosa in patients with various gastrointestinal disorders. Duodenal gastrin concentration was 5.9±1.2 ng/mg (mean ±1sem) in control patients. Duodenal gastrin concentration was similar to control values in patients with duodenal ulcer, pyloric channel ulcer, vagotomy and pyloroplasty, and gastric atrophy and hypergastrinemia. In gastric ulcer patients, duodenal gastrin concentration, 2.8±0.6 ng/mg, was significantly less than the control value (P<0.05). Duodenal gastrin concentration was approximately one third of antral gastrin concentration in control, duodenal ulcer, and gastric ulcer patients and was approximately one fifth of antral gastrin concentration in vagotomy and pyloroplasty patients and gastric atrophy patients. Duodenal and antral gastrin concentrations were significantly correlated in normal controls and in gastric ulcer patients. The finding of normal duodenal gastrin concentration in patients with vagotomy and pyloroplasty and patients with gastric atrophy suggests that, unlike antral gastrin concentration, duodenal gastrin concentration is unaffected by a decrease in acid secretion rate. The low duodenal gastrin concentration in gastric ulcer patients indicates that the duodenum may be involved in the pathophysiology of gastric ulcer disease.This work was supported in part by Clinical Research Center grant RR-00093, U.S. Public Health Service, Washington, D.C.     

Interdigestive Gastroduodenal Motility in Duodenal Ulcer: Role of Gastric Acid Hypersecretion

The interdigestive gastroduodenal motility was studied by means of a multilumen manometric probe in eight patients with active duodenal ulcer (group DU1) and in seven patients with hypersecretory gastroduodenitis (group GD). Both groups were selected on the basis of the presence of gastric acid hypersecretion. A group of five patients with non-active duodenal ulcer (group DU2) and a group of eight healthy subjects (group C) also were examined. Both of the latter groups were selected on the basis of the presence of normal gastric secretion. After a basal recording period of 200-300 min, in hypersecretory groups DU1 and GD, ranitidine was administered to decrease acid secretion; in normosecretory groups C and D2, impromidine was infused at two scalar doses to increase acid secretion. The basal recording showed in groups DU1 and GD a longer than normal time interval between consecutive activity fronts (AF) of the migrating motor complex (MMC cycle) and a shorter than normal percent of time occupied by AFs. In normal subjects and in DU2, the administration of the lowest dose of impromidine induced a motor pattern similar to that of the basal period of groups DU and GD, whereas the highest dose disrupted the MMC pattern that was replaced by an irregular motor activity. The results of this study indicate that duodenal ulcer with acid hypersecretion shows a marked inhibition of the MMC cycle that is not due to the ulcer itself, but to the increased acid secretion. In fact, the same motor pattern is observed in other hypersecretory states, both spontaneous and drug-induced, whereas DU with normal secretion showed a near normal motility. In active duodenal ulcer, the decreased incidence and duration of activity fronts may play a role in the pathogenesis of peptide ulcer, as it may impair the cyclic duodenal acid clearing, allowing a longer than normal contact of HCl with the duodenal mucosa.     

Nocturnal gastric acid secretion in duodenal ulcer: inhibition by cimetidine

The inhibitory effect of cimetidine 200 mg, cimetidine 400 mg, cimetidine 200 mg + oxyphenonium bromide 10 mg and placebo was studied on nocturnal gastric acid secretion in 10 patients with duodenal ulcer. Each patient was studied over a period of four nights and trial medication was given in a randomized sequence. Cimetidine in both doses significantly inhibited the nocturnal gastric acid secretion. The drug reduced both the H+ concentration and gastric juice volume but the reduction of H+ concentration was more impressive. Mean percentage inhibition of nocturnal acid output with cimetidine 400 mg (89.6 +/- 2.868) was significantly higher than cimetidine 200 mg (80.3 +/- 4.085; p less than 0.01). Combination of cimetidine 200 mg and oxyphenonium bromide 10 mg was significantly better than cimetidine 200 mg alone (p less than 0.05) and this combination produced inhibition of gastric juice volume, H+ concentration and acid output comparable to cimetidine 400 mg.     

Duodenal pH in health and duodenal ulcer disease: effect of a meal, Coca-Cola, smoking, and cimetidine

Intraluminal duodenal pH was recorded using a combined miniature electrode and logged digitally every 10 or 20 seconds for five hours (basal/meal/drink) in eight control subjects and 11 patients with duodenal ulcer (five on and off treatment with cimetidine). Over the whole test there were no significant differences in duodenal mean pH or log mean hydrogen ion activity (LMHa) between control subjects and patients with duodenal ulcer, but there were significantly longer periods of duodenal acidification (pH less than 4) and paradoxically more periods of duodenal alkalinisation (pH greater than 6) in the duodenal ulcer group compared with controls. After a meal duodenal mean pH and LMHa fell significantly in both controls and patients with duodenal ulcer, with more periods of duodenal acidification and alkalinisation in the duodenal ulcer group. An exogenous acid load (Coca-Cola) significantly increased the periods of duodenal acidification, and reduced alkalinisation, in both groups. Cimetidine significantly increased mean pH and LMHa and abolished the brief spikes of acidification in four of five patients with duodenal ulcer. Peak acid output (but not basal acid output) was significantly correlated with duodenal mean pH and LMHa but not with the periods of duodenal acidification. Smoking did not affect duodenal pH in either group.     

Gastric pepsin and acid secretion in patients with acute and healed duodenal ulcer

The relationship between gastric pepsin, acid secretion, and duodenal ulcer activity was studied in 33 patients with an endoscopically proven carter, in 17 patients who were studied within 3 mo of an acute crater but who no longer had a crater endoscopically, and in 10 patients who had no duodenal ulcer symptoms for longer than 3 mo after a crater and who had negative endoscopy. There were an additional 11 patients who had paired studies in the early-healed and late-healed stages of their disease. There were no significant differences between the values obtained in the paired and nonpaired group. Basal and pentagastrin-stimulated outputs of both pepsin and acid were significantly higher (p less than 0.001) when an acute crater was present than in 23 control subjects. At 3 mo or more after healing there was a significant (p less than 0.001) fall in both basal and stimulated pepsin and acid output which became insignificantly different from that of controls. In 104 basal studies the ratio of pepsin to acid secretion was 33,000 +/- 2500 (mean +/- SE) pepsin units/mmol H+ with no difference between any groups including controls. In 102 stimulated studies the ratio was 13,600 +/- 400 PU/mmol H+, also with no differences between any groups. Although data in the literature are conflicting, these results support a direct relationship between the activity of duodenal ulcer disease and acid-pepsin secretion.     

Duodenal ulcer

Although the etiology of duodenal ulcer is not known, its treatment with drugs that reduce acid secretion is well accepted. The central role of calcium in stimulus-secretion coupling resulting in acid secretion by gastric parietal cells is documented. However, the status of intracellular calcium in gastric parietal cells in the basal state in patients with duodenal ulcer is not known. Multiple endoscopic gastric mucosal biopsies from the corpus of the stomach of 52 patients were processed and isolated parietal cells were studied. Intracellular calcium was estimated using fura-2-acetoxymethyl ester. Influx and efflux were determined by using radioactive calcium. Acridine orange retention was used to assess acid production. Only calcium influx at 20 min was significantly (P<0.01) more in patients with duodenal ulcer as compared to the control group. There was no difference between the groups in calcium influx at 0 and 60 min; calcium efflux at 0, 20, and 60 min; intracellular free calcium and acid secretion. We conclude that in the unstimulated state calcium homeostasis in isolated parietal cells of patients with duodenal ulcer shows only a minimal difference as compared to controls.     

Different HCl and Pepsinogen I Secretion Patterns in Anatomically Defined Gastric Ulcer Subsets

Anatomically, functionally, and clinically, peptic ulcer patients are a heterogeneous group of subjects. These patients can be classified according to the anatomic localization of the niche. The functional state of the gastric mucosa was studied in 30 gastric ulcer patients, 25 duodenal ulcer patients, and 10 normal controls. The classification of the first group was based on Johnson's criteria, with the following results: 10 individuals were type I, 10 were type II, and 10 were type III. Pepsinogen I levels and gastric acid secretion were measured in all 65 subjects under basal conditions and after subcutaneous pentagastrin stimulation. Both basal and stimulated serum pepsinogen I values were significantly higher (p less than 0.05) in gastric ulcer type III patients than in the other four groups. These values in gastric ulcer type I were similar to those of the controls. Gastric ulcer type II patients showed an intermediate functional state similar to that of duodenal ulcer patients. In both gastric ulcer type II and duodenal ulcer patients, the basal and stimulated pepsinogen I levels were significantly higher (p less than 0.05) than those found in controls, whereas the basal serum gastrin levels were similar in the five groups. In conclusion, different HCl and pepsinogen I secretory patterns, with functional heterogenicity of the gastric mucosa, are shown here for the anatomically defined gastric ulcer subsets.     

Lysolecithin and Glyceroglucolipids in Gastric Secretion of Patients with Gastric and Duodenal Ulcer

Basal and pentagastrin-stimulated gastric secretions, collected (at 15-min intervals for 1 h) from six duodenal ulcer and six gastric ulcer patients, were analyzed for their content of lecithin, lysolecithin, and glyceroglucolipids. Whereas the glycero-glucolipid concentrations and the molar ratios of lysolecithin to lecithin (2.5:1) in basal and stimulated secretions from patients with duodenal and gastric ulcer were similar, significant (p < 0.01) differences were noted between these two groups with regard to the lysolecithin contents. The basal secretions of patients with duodenal ulcer contained about 4.5-fold less (204 μmol/l) of lysolecithin than those from patients with gastric ulcer (932 μmol/l). After pentagastrin stimulation, the lysolecithin concentrations in the secretion from duodenal ulcer patients rose slightly (to 212 μmol/l), whereas a twofold decrease (to 440 μmol/l) in lysolecithin was observed in the secretion from patients with gastric ulcer. Statistically significant correlation between concentrations of lysolecithin and glyceroglucolipids was only observed in basal (r = 0.85, p < 0.05) and stimulated (r = 0.93, p < 0.01) secretions from patients with gastric ulcer. It is concluded that high concentrations of lysolecithin in the secretion of gastric ulcer patients results in the weakening of the gastric mucosal barrier by depleting its glyceroglucolipid component.     

Acid, pepsin, and mucus secretion in patients with gastric and duodenal ulcer before and after colloidal bismuth subcitrate (De-Nol).

Basal and pentagastrin stimulated gastric secretion was measured in seven patients with duodenal, and six with gastric ulcers before and after four weeks' treatment with colloidal bismuth subcitrate (as De-Nol), one tablet four times a day. Each duodenal and all but one of the gastric ulcers healed. After De-Nol there were no significant changes in basal, or pentagastrin stimulated volume, acid output, or primary parietal component. There were marked decreases in basal (duodenal ulcer -25%; gastric ulcer -16%) and pentagastrin stimulated total pepsin outputs, (duodenal ulcer -42%, gastric ulcer -36%). There were insignificant decreases in basal output of mucus, but postpentagastrin stimulated mucus output was significantly inhibited (p less than 0.05) in patients with duodenal (-16%) and with gastric ulcer (-27%). The drop in gastric proteolysis after De-Nol is unlikely to be because of the healing of the ulcers and is more likely to be because of the drug. The ulcer healing efficacy of De-Nol may be related to this decline in the proteolytic action of gastric juice, but is unlikely to be because of a quantitative change in mucus, or in acid secretion.     

Release of pancreatic polypeptide in response to the intragastric administration of a meal is not different in duodenal ulcer patients and normal subjects

The high basal and meal-induced acid secretions in duodenal ulcer patients has led to the concept that vagal hyperactivity is a common factor in the pathogenesis of peptic ulcer. For these reasons, since pancreatic polypeptide secretion is known to be under vagal control, we studied the pancreatic polypeptide release after intragastric administration of two protein meals (10 and 20 g protein in 400 ml) in 18 duodenal ulcer patients and in 17 normal subjects. After a 10 g protein meal was administered, gastric pH was either maintained at pH 4.5 or allowed to decrease. The 20 g protein meal induced a higher pancreatic polypeptide release than did the 10 g protein meal (p less than 0.05): the integrated pancreatic polypeptide responses were 1.07 +/- 0.5 and 3.21 +/- 0.58 nmol/l/60 min respectively in the duodenal ulcer group and 0.46 +/- 0.21 and 2.67 +/- 0.69 nmol/l/60 min respectively in the control group. On the other hand, the responses to the two protein meals in duodenal ulcer patients were not different from those obtained in normal subjects, despite the higher meal-induced acid secretions in the duodenal ulcer group. pancreatic polypeptide increase was not larger when gastric pH was fixed than when it was allowed to decrease, 0.56 +/- 0.21 and 1.7 +/- 0.63 nmol/l/60 min respectively in normal subjects and 1.07 +/- 0.5 and 1.07 +/- 0.49 nmol/l/60 min respectively in duodenal ulcer patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of parietal cell vagotomy on acid secretory responsiveness to circulating gastrin in humans. Relationship to postprandial serum gastrin concentration

To study the relationship between gastric acid secretion and serum gastrin concentration after vagotomy, gastric acid output and serum gastrin concentration were measured simultaneously during intravenous infusion of graded doses of human gastrin heptadecapeptide (G-17) in duodenal ulcer patients with parietal cell vagotomy and in unoperated patients with duodenal ulcer disease (controls). The curve relating serum gastrin concentration to gastric acid output was shifted downward and to the right after vagotomy; the peak acid output to G-17 was reduced by 50% (p less than 0.001). The serum gastrin concentration that produced half of peak acid output (EC50%) averaged 185.5 pg/ml after vagotomy and 74.1 pg/ml in controls (p less than 0.01). Mean basal and postprandial serum gastrin concentrations were twofold to threefold higher in vagotomy patients than in controls (p less than 0.005). However, when peak postprandial serum gastrin concentrations were used to predict acid secretion from curves relating serum gastrin to acid output, predicted acid secretion was only 12.6 mmol/h in vagotomy patients compared to 24.4 mmol/h in controls. Parietal cell vagotomy decreases "functional" parietal cell mass, as reflected by a 50% decrease in peak acid output, and also reduces the responsiveness of "functional" parietal cells to gastrin to such an extent that acid secretion is reduced after vagotomy despite basal and postprandial hypergastrinemia.     

Altered solid and liquid gastric emptying in patients with duodenal ulcer disease.

Alteration in gastric emptying has been implicated in duodenal ulcer disease. The precise abnormalities remain controversial. We have used a radionuclide technique to assess solid and liquid gastric emptying in 14 patients with endoscopically proven duodenal ulcer and 22 healthy controls. Solid gastric emptying values for the patient group fell within the normal range. The median time taken for 50% (T50) of the liquid marker to empty from the stomach was 12 minutes (range 6-23 minutes) which was significantly faster (p less than .005) than controls (median 18 minutes, range 11-35). In 10 of the 14 patients, however, the rate of liquid emptying was within the normal range. There was no significant difference in the T50 for gastric emptying of solids between the groups, but in duodenal ulcer patients food left the stomach significantly earlier than in controls (p less than .05). After this, however, the linear rate at which duodenal ulcer patients emptied solid food from the stomach was a median 0.75%/minutes (range 0.5-1.4 minutes), which was slower (p less than .0005) than controls, median 1.25/minutes (range 0.7-2.3). These results show that the pattern of gastric emptying of digestible solids and liquids in patients with duodenal ulcer disease, as a group, is significantly altered.     

Effect of low-dose exogenous secretin and somatostatin on pentagastrin-stimulated gastric acid secretion in man

The inhibitory effect of intravenous infusion of secretin (0.05 CU kg-1h-1) and somatostatin (60 pmol kg-1h-1), given alone or in combination, on pentagastrin-stimulated (100 ng kg-1 h-1) acid secretion was studied in 10 healthy subjects. Secretin inhibited acid secretion by 54% (p less than 0.05), and somatostatin inhibited by 70% (p less than 0.05). The combined infusion of secretin and somatostatin decreased acid output by 64% (p less than 0.05). The differences between the three groups were not significant (p greater than 0.05). Median plasma concentrations of secretin and somatostatin were of the same magnitude as seen after duodenal acidification. The present study did not demonstrate any interaction between secretin and somatostatin in the inhibition of gastric acid secretion.