Basal Serum Gastrin Concentrations Research Articles

Significance of an exaggerated meal-stimulated gastrin response in pathogenesis of Helicobacter pylori-negative duodenal ulcer.

The aim of this study was to clarify the pathogenesis of Helicobacter pylori-negative duodenal ulcer (DU) by investigating the meal-stimulated serum gastrin (SG) response. The subjects were 9 patients with H. pylori-negative DU, 28 H. pylori-positive DU, 11 H. pylori-positive volunteers, and 30 H. pylori-negative volunteers. Blood samples were taken before and after consumption of a test meal. The integrated 1-hr gastrin response (IGR) was taken to be the area under the SG time curve, calculated by the trapezoid method. H. pylori infection status was determined by histology, serology, and the [13C] urea breath test. The mean basal SG concentration was lower in the H. pylori-negative DU patients than in the H. pylori-positive DU patients, but an exaggerated IGR was observed in three patients (33.3%) with H. pylori-negative DU. In conclusion, our findings indicate that an exaggerated meal-stimulated gastrin response may contribute to the pathogenesis of H. pylori-negative DU.

Gastrinaemia, Tissue Gastrin Concentration and G Cell Density in the Antral Mucosa of Swine With and Without Gastric Ulcer of the Pars Oesophagea

Gastric ulcer of the pars oesophagea (GUPO) of the stomach, which occurs spontaneously in swine, is of unknown aetiology. Because gastrin is a potent secretagogue linked to acid secretion, this study was designed to investigate, in pigs with or without GUPO, (1) basal and food-stimulated serum gastrin concentrations, (2) the concentration of tissue gastrin, and (3) gastrin-producing (G) cell density in the antral mucosa. Sixty-four pigs (32 with, and 32 without ulceration) were studied. Antral mucosa was obtained immediately after slaughter for assessment of G-cell number and tissue gastrin concentration. The presence or absence of GUPO was not significantly associated with either of the parameters measured.

Rectal cell proliferation and colon cancer risk in patients with hypergastrinaemia

Background—The influence of gastrin on the colonic mucosa is still uncertain. Some authors have suggested a stimulating effect on the growth of normal and malignant colonic epithelium, while others have...

Chronic systemic treatment with epidermal growth factor induces hypergastrinaemia in Goettingen minipigs.

Epidermal growth factor (EGF) is an inhibitor of gastric acid secretion. The impact of chronic systemic treatment with EGF on intragastric pH and serum gastrin concentrations has not been investigated previously. Goettingen minipigs were treated with human recombinant EGF (hEGF) or placebo for 4 weeks. Once a week the acidity and protein concentration of gastric juice were determined, and serum gastrin concentrations measured. After 4 weeks, tissue specimens were obtained from the gastric antrum and immunostained for gastrin- and somatostatin-producing G- and D-cells. Furthermore, the development of antibodies against hEGF was evaluated. Subcutaneously administered hEGF, 30 micrograms/kg/day for 4 weeks, included a fourfold increase in basal serum gastrin concentration, increased the number of antral G-cells, and decreased the density of antral D-cells. The acidity of gastric fluid was reduced, and the protein concentration increased. All animals developed low-titred antibodies towards hEGF. The antibodies did not influence the extent to which the individual animal responded to the EGF treatment.

Eradication of Helicobacter pylori infection in patients with non-ulcer dyspepsia. Effects on basal and bombesin-stimulated serum gastrin and gastric acid secretion.

This study evaluates the effect of eradicating Helicobacter pylori on basal and bombesin-stimulated gastric acid secretion and serum gastrin in non-ulcer dyspepsia. Before and 1 month after an attempt to eradicate H. pylori basal and bombesin-stimulated gastric acid outputs were measured in 23 patients. H. pylori was eradicated in 15 patients (group A) but not in the other 8 (group B). Incremental gastric acid output was calculated by subtracting basal from bombesin-stimulated values. Basal acid output increased significantly (p = 0.01) after therapy in group A (delta 1.6 +/- 0.6 mmol/h) but not in group B (delta 0.2 +/- 0.5 mmol/h). Incremental gastric acid output decreased distinctly (delta-3.9 +/- 1.4 mmol/h) after therapy in group A (p = 0.02) but not in group B (delta-2.2 +/- 1.7 mmol/h). Basal serum gastrin decreased significantly (p < 0.005) after therapy in group A (delta-9 +/- 4 pM) but not in group B (delta-1 +/- 2 pM). Integrated serum gastrin responses to bombesin decreased markedly (p < 0.001) after therapy in group A (delta-5.0 +/- 1.6 nM*60 min) but slightly in group B (delta-0.9 +/- 1.3 nM*60 min) (p < 0.05). In patients with non-ulcer dyspepsia basal serum gastrin concentrations decrease but basal gastric acid outputs increase after eradication of H. pylori. Bombesin-induced increments in gastric acid output, however, decrease in parallel with gastrin release.

Serum gastrin and mucosal somatostatin in Helicobacter pylori-associated gastritis.

The aims were to study gastrin concentrations and gastric mucosal somatostatin and gastrin concentrations in relation to the extent of gastritis in Helicobacter infection. We measured basal serum gastrin concentrations in antral mucosal biopsy specimens and somatostatin concentrations in corpus biopsy specimens in 88 consecutive dyspeptic subjects undergoing endoscopy. These subjects were divided into three categories on the basis of histology, serology, and culture: H. pylori-positive pangastritis, H. pylori positive antral gastritis with normal body histology, and H. pylori-negative controls. Statistical evaluation was done with the Wilcoxon rank sum test. Basal serum gastrin concentrations were significantly increased only in subjects with pangastritis and not in those with antral gastritis only, as compared with controls (mean +/- SEM: 72 +/- 7, 46 +/- 10, and 42 +/- 7 ng/l, respectively). Subjects with pangastritis or antral gastritis had significantly lower antral somatostatin concentrations than controls (mean +/- SEM: 0.80 +/- 0.07, 1.03 +/- 0.15, and 2.40 +/- 0.31 micrograms/g(protein), respectively). We also found significantly lower antral gastritis only as compared with controls (mean +/- SEM: 62 +/- 13, 78 +/- 16, and 165 +/- 25 micrograms/g(protein), respectively). In subjects with pangastritis a significantly lower concentration of somatostatin was found in the corpus biopsy specimens than in those with antral gastritis only and controls. These results suggest that hypergastrinemia in H. pylori gastritis is not caused by antral gastritis and antral somatostatin deficiency alone but that corpus inflammation plays a key role in the origin of hypergastrinemia. Furthermore, in patients with pangastritis a corpus mucosal somatostatin deficiency was found.

Effect of enprostil on serum gastrin and pepsinogen A and C levels in patients on long‐term treatment with omeprazole

Treatment of omeprazole induces profound inhibition of gastric acid secretion, resulting in hypergastrinaemia. In rats hypergastrinaemia induced by chronic administration of high doses of omeprazole resulted in ECL-cell hyperplasia and subsequent carcinoid formation. This finding may limit long-term therapy in man. The synthetic prostaglandin E2 analogue enprostil not only inhibits gastric acid secretion but also reduces serum gastrin in normal subjects and in peptic ulcer patients. The present study was undertaken to determine whether enprostil reduces serum gastrin in patients on long-term treatment with omeprazole. Eight patients with reflux oesophagitis treated with 40 mg omeprazole once daily for at least 3 months received 35 micrograms enprostil t.d.s. during a 5-day treatment course. Basal and postprandial serum gastrin concentrations and pepsinogen A and C levels were measured on the day before, the first and the final day, and on the day after cessation of treatment. Enprostil significantly (P < 0.05) reduced basal serum gastrin from 65 +/- 15 pmol/L to 51 +/- 13 pmol/L on the first treatment day, and to 41 +/- 9 pmol/L on the final day. Enprostil also significantly (P < 0.05) reduced postprandial integrated serum gastrin from 6173 +/- 849 pmol.h/L to 4516 +/- 906 pmol.h/L and to 3532 +/- 706 pmol.h/L on the first and final treatment days, respectively. On the day after cessation of treatment basal (57 +/- 11 pmol/L) and postprandial integrated serum gastrin concentrations (5766 +/- 864 pmol.h/L) were not significantly different when compared to pretreatment values. Enprostil had no significant influence on serum pepsinogens A and C. Short-term co-administration of enprostil lowers the serum gastrin levels in patients on long-term treatment with omeprazole.

Effect of loxiglumide on basal and gastrinand bombesin-stimulated gastric acid and serum gastrin levels

The effect of the specific cholecystokinin-receptor antagonist loxiglumide on basal and bombesin-, and gastrin 17-I-stimulated gastric acid secretion and serum gastrin levels was studied in 12 healthy subjects. Loxiglumide (10 mg · kg−1 · h−1) significantly augmented basal gastric acid output from 1.8 ± 0.3 to 3.9 ± 0.6 mmol H+/h (P < 0.005) but did not significantly influence integrated basal serum gastrin concentrations (2 ± 21 vs. 32 ± 21 pmol L−1 · h−1). Both gastric acid secretion and integrated serum gastrin concentrations stimulated by bombesin infusion (92.6 pmol · kg−1 · h−1) were significantly augmented by loxiglumide [from 4.0 ± 0.3 to 10.0 ± 1.3 mmol H+/h (P < 0.005) and from 1251 ± 93 to 2558 ± 206 pmol · L−1 · h−1 (P < 0.005), respectively]. Gastric acid output and serum gastrin concentrations during infusion of 5 pmol · kg−1 · h−1 of synthetic human gastrin 17-1 (9.6 ± 2.9 mmol H+/h and 1045 ± 177 pmol · L−1 · h−1) and during infusion of 15 pmol · kg−1 · h−1 of gastrin 17-I (14.5 ± 3.1 mmol H+/h and 2412 ± 312 pmol · L−1 · h−1) were not significantly influenced by loxiglumide (10.3 ± 2.3 mmol H+/h and 1291 ± 257 pmol · L−1 · h−1 for the 5-pmol · kg−1 · h−1 gastrin 17-I infusion dose with loxiglumide and 13.6 ± 3.4 mmol H+/h and 2611 ± 305 pmol · L−1 · h−1 for the 15-pmol · kg−1 · h−1 gastrin 17-I infusion dose with loxiglumide). These data indicate that endogenous cholecystokinin inhibits gastric acid secretion under basal conditions and gastrin release and gastric acid secretion during infusion of bombesin in humans and suggest that the augmented effect of loxiglumide on bombesin-stimulated gastric acid secretion may be explained largely by enhanced gastrin release.

Role of affect and personality in gastric acid secretion and serum gastrin concentration: Comparative studies in normal men and in male duodenal ulcer patients

The role of mood state (affect) and personality on basal acid secretion and basal serum gastrin concentrations were examined in seven healthy men and eight patients with duodenal ulcer. In each subject, gastric secretion and affect were assessed simultaneously on 5 separate days. None of 10 selfreported affect variables correlated with daily fluctuations in basal acid secretion in either group. Three variables (tension, conflict, and anxiety) correlated significantly with serum gastrin fluctuations in normal subjects, but these relationships were not present in patients with ulcer, who were hypergastrinemic regardless of their affective state. The degree to which serum gastrin fluctuated was unrelated to personality, as assessed by Minnesota Multiphasic Personality Inventory. On the other hand, several Minnesota Multiphasic Personality Inventory scales correlated with the degree of variability in basal acid secretion, including scales that measured impulsivity and social isolation/alienation. These studies indicate that serum gastrin concentrations are related to affective state in normal men, that this relationship is altered in men with duodenal ulcer, and that certain personality traits, such as impulsivity and social isolation, are associated with more labile basal acid secretion rates.

Gastric acid and pepsin hypersecretion in conscious rabbits

In conscious, gastric fistula rabbits, gastric acid and pepsin secretion averaged 4.5 +/- 0.1 mmol/h (1.3 mmol.kg-1.h-1) and 4.9 +/- 0.3 IU/h (1.6 IU.kg-1.h-1), respectively; these values represent approximately 40-50% of maximal output. Basal serum gastrin concentrations averaged 24 +/- 4 pg/ml and did not correlate with basal acid secretion. Atropine and vagotomy incompletely inhibited basal acid secretion (by 84 and 50%, respectively) and completely inhibited 2-deoxy-D-glucose-stimulated gastric acid secretion. Atropine and vagotomy similarly inhibited basal pepsin secretion by 50 and 40%, respectively. Ranitidine decreased acid and pepsin secretion, but as with atropine, inhibition was not complete (73 and 37%, respectively). Although omeprazole did not affect pepsin secretion, omeprazole completely inhibited basal acid secretion and elevated postprandial intragastric pH above 5.0. Conscious, gastric fistula rabbits have the highest basal acid and pepsin output among species commonly studied. Both vagal-cholinergic pathways and histamine drive basal acid and pepsin secretion in the rabbit.

Gastric Acid Secretion in Basenji Dogs With Immunoproliferative Enteropathy

Gastric acid secretion was studied in 13 Basenji dogs with immunoproliferative enteropathy. Considerable variation in the severity of gastritis and enteritis existed among dogs. Basenji dogs were categorized into two groups on the basis of postmortem gastric and intestinal histology (group I, gastritis and enteritis; group II, only enteritis). Pentagastrin-induced gastric acid secretory capacity was increased (P less than 0.002) in group II dogs as compared to healthy Beagle controls. Gastric acid secretory capacity of Basenji dogs with gastritis and enteritis (group I) was not different from that observed in control dogs. Basal serum gastrin concentrations and secretin-stimulated serum gastrin concentrations of either group of Basenji dogs did not differ from controls. On the basis of symptomatology, Basenji dogs with diarrhea had significantly increased basal and postsecretin stimulation gastrin concentrations (P = 0.01) when compared with asymptomatic Basenji or healthy control dogs. These findings support a potential role for altered gastric acid secretory capacity in the pathogenesis of immunoproliferative enteropathy of Basenji dogs. Results of the secretin stimulation studies support previous pathologic studies that failed to detect gastrin-secreting tumors. Incorporated into this investigation was a trial to determine whether the combination of oxymorphone and acepromazine could be used for acid secretory studies. Compared to pentobarbital, which has been frequently used for acid secretory studies in a research setting, the drug combination resulted in increased gastric fluid volumes, a comparative increase in acid secretion, and a rapid uneventful recovery. We conclude that the combination of oxymorphone and acepromazine provides an acceptable means of restraint in dogs undergoing acid secretory studies.

Omeprazole 20 mg three days a week and 10 mg daily in prevention of duodenal ulcer relapse: Double-blind comparative trial

In a double-blind, parallel-group clinical trial of 195 patients with duodenal ulcers who after a short-term study had relief of pain and healed ulcers proved endoscopically, 65 were randomized to receive 20 mg omeprazole 3 days a week (once in the morning from Friday to Sunday), 64 to receive 10 mg omeprazole once daily in the morning, and 66 to receive placebo for up to 6 months. The patients underwent repeat endoscopy with biopsy of the gastric fundic mucosa (qualitative assessment of argyrophilic cell population), assessment of symptoms, and laboratory screening with measurement of basal serum gastrin concentrations at 3 and 6 months or more often if indicated by recurrence of symptoms. At 3 months, endoscopically proved ulcer relapse occurred in 16% receiving 20 mg omeprazole 3 days a week; 21% receiving 10 mg omeprazole daily; and 50% receiving placebo. At 6 months, corresponding rates were 23%, 27%, and 67% with 95% confidence intervals of difference between the placebo group and omeprazole groups of 28%-60% and 24%-56% (P less than 0.00001), respectively, and between omeprazole groups of -19%-11% (NS). No major clinical or laboratory side effects were noted. Thus both omeprazole regimens are effective and safe in preventing duodenal ulcer relapse.

Effect of truncal vagotomy on parietal cell mass and antral gastrin cell mass in dogs

Vagotomy is known to reduce acid secretion and to increase serum gastrin concentrations. However, there is minimal information on the effect of vagotomy on parietal cell mass or gastrin cell mass. Basal and maximal acid secretions and fasting serum gastrin concentrations were measured in 22 gastric fistula dogs with pyloromyotomy before and up to 56 days following complete bilateral truncal vagotomy (n = 11) or sham vagotomy (n = 11). Dogs underwent total gastrectomy on postoperative day 9 (n = 5 per group) or day 56 (n = 6 per group). Parietal cells were stained with Luxol fast blue and parietal cell mass determined with computer-assisted histomorphometry. Parietal cell mass averaged 10.68 ± 0.90 billion in control dogs and correlated significantly with maximal acid output (r = 0.76; P < 0.01). Vagotomy reduced maximal acid output by 40%–50% (P < 0.001) but had no significant effect on parietal cell mass (8.99 ± 1.00 billion). Vagotomy increased serum gastrin concentrations significantly, but antral gastrin cell mass in vagotomized dogs (5.66 ± 1.00 million) was not significantly different than that in control dogs (4.74 ± 0.50 million). Thus, vagotomy did not lead to parietal cell hypoplasia or gastrin cell hyperplasia despite profound alterations in parietal cell and gastrin cell function.

High Doses of Ranitidine in Patients with Reflux Oesophagitis

As in duodenal and gastric ulcer patients, a highly significant correlation between suppression of 24-h intragastric acidity and healing rates in reflux oesophagitis patients was demonstrated by meta-analysis of data obtained from the literature (r = 0.90; p less than 0.001). Furthermore, we have demonstrated in eight patients with reflux oesophagitis that 2-week treatment courses with 300 mg ranitidine twice daily and 300 mg four times daily progressively decreased 24-h intraoesophageal acidity but only moderately elevated basal and meal-stimulated serum gastrin concentrations, significantly below gastrin values obtained after a 2-week treatment course with 20mg omeprazole once daily. Further studies are awaited to demonstrate long-term effects on both healing rates and serum gastrin responses with high doses of histamine H2-receptor antagonists.

Role of Aggressive Factors in the Pathogenesis of Peptic Ulcer Disease

Acid and pepsin are the major aggressive factors believed to play a role in the pathogenesis of peptic ulcer disease. On the average, patients with duodenal ulcer disease have higher than normal basal, nocturnal, and pentagastrin-stimulated acid secretion. Food-stimulated acid secretion, however, is normal in duodenal ulcer patients. The reason for higher basal and nocturnal acid secretion is not known but may be secondary to higher than normal basal serum gastrin concentrations in duodenal ulcer patients. Average serum pepsinogen levels also are higher than normal in patients with duodenal ulcer disease, suggesting that luminal pepsin concentrations also are higher. Patients with gastric ulcers have either normal or lower than normal acid secretion. This suggests that factors other than acid and pepsin may play a role in causing gastric ulcers. Reflux of bile and pancreatic juice into the stomach of patients with gastric ulcers has been suggested as one of the aggressive factors playing a role in the development of gastric ulcers.

Gastrin and the vagus interact in the trophic control of the rat oxyntic mucosa

Gastrin is a trophic hormone for the stomach, and permanent reduction of circulating gastrin by antrectomy leads to atrophy of the oxyntic mucosa, including a reduced density of histamine-storing endocrine cells (so-called ECL cells). Recently, it was proposed that also the vagal nerve has a trophic influence on the stomach. The two vagal trunks innervate the anterior and posterior side of the gastric wall, respectively. This arrangement makes it possible to denervate one side of the stomach selectively. The objective of the present study was to examine the consequences of combined antrectomy and vagotomy (unilateral or bilateral). Male Sprague-Dawley rats were subjected to unilateral or bilateral subdiaphragmatic truncal vagotomy with or without antrectomy. Control rats were sham-operated. The rats were killed 8 weeks after the operation. Bilateral vagotomy raised the basal serum gastrin concentration (fasting level). The thickness of the oxyntic mucosa and the density of ECL cells were not significantly different from age-matched vagally intact controls. Unilateral vagotomy induced no change in the basal serum gastrin concentration, nor did it affect the mucosa on the intact side. On the denervated side, however, there was reduced mucosal thickness and a greatly reduced ECL cell density. With a combination of antrectomy and vagal denervation the decrease in ECL cell density was exaggerated compared to the effect of antrectomy or unilateral vagotomy alone. The results suggest that gastrin and the vagus interact synergistically to maintain the normal integrity of the rat oxyntic mucosa and that the ECL cells represent an important target for both gastrin and the vagus.

Effect of intermittent weekend therapy with omeprazole on basal and postprandial serum gastrin concentrations in patients with duodenal ulcer.

We have studied the effect on serum gastrin concentrations of weekly 3-day courses of 20 mg/day omeprazole followed by a 4-day period without medication (weekend therapy) for 4 weeks in 10 patients with duodenal ulcer. Basal and postprandial serum gastrin concentrations were measured in week 1, before (day 1) and immediately after the 3-day omeprazole course (day 4), and further on day 6 and day 8, immediately before the next course, and at similar intervals in week 4 (days 22, 25, 27, and 29). Basal serum gastrin concentrations were not significantly different from day 1, but postprandial peak gastrin concentrations on days 6, 8, 22, 25, 27, and 29 and integrated postprandial gastrin secretion on days 25 and 27 were significantly increased (p less than 0.01 to p less than 0.05). However, the increases in serum gastrin concentration were modest and clinically irrelevant. It is concluded that this intermittent weekend schedule of omeprazole therapy does not induce marked hypergastrinemia and may therefore be suitable for long-term therapy with this drug.

The fasting and food-stimulated serum gastrin concentration in 151 duodenal ulcer patients compared to 41 healthy subjects

The basal and postprandial serum gastrin concentrations (SGC) were compared between 151 duodenal ulcer (DU) patients and 41 non-dyspeptic volunteers. All DU patients had an eventful history and were submitted to us for surgery. The basal SGC was significantly higher in DU patients (40 ± 30 vs 17 ± 8 pg/ml). The peak postprandial SGC was also significantly higher (123 ± 83 vs 52 ± 28 pg/ml) and the intergrated gastrin output twice as high as in healthy subjects (5311 ± 3879 vs 2554 ± 1995 pg/ml × min; P < 0.01). A statistically significant liniar correlation for fasting and maximal postprandial SGC was found. No statistically significant interrelation between gastrin and acid parameters existed. In the DU patients no differences in SGC were found according to age. Fifteen patients complained of non-alimentary vomiting as part of their ulcer symptoms. They had significantly higher SGC although no differences in acid secretion were found. No significant differences in gastrin or acids were related to ulcer complications.

Effect of GABA on basal and vagally mediated gastric acid secretion and hormone release in dogs.

To stimulate peripheral gamma-aminobutyric acid (GABA) receptors, GABA, which does not cross the blood-brain barrier, was administered to dogs with vagally innervated gastric fistulas at intravenous doses of 0, 0.66, 2, 6, 18, and 54 micrograms.kg-1.min-1. Mean gastric acid output increased from zero basally to 3.0 +/- 1.4 mmol/h during infusion of 54 micrograms.kg-1.min-1 GABA. Plasma somatostatin-like immunoreactivity decreased significantly below basal levels during infusion of 54 micrograms.kg-1.min-1 GABA (P less than 0.05). To stimulate central nervous system GABA receptors as well as peripheral GABA receptors, progabide, a GABA-receptor agonist, which readily crosses the blood-brain barrier, was injected intravenously. Mean acid output was 3.5 +/- 1.3 mmol/h after 20 mg/kg progabide and 0.6 +/- 0.5 mmol/h after its vehicle (P less than 0.05). Basal serum gastrin concentration increased significantly after progabide injection. Acid output during insulin-induced hypoglycemia was inhibited 59% by 30 mg/kg intravenous progabide. Progabide infusion also diminished or abolished circulating gastrin, somatostatin, and pancreatic polypeptide responses during insulin-induced hypoglycemia (P less than 0.05). Further studies were performed in dogs with a gastric fistula and a vagally denervated Heidenhain pouch to confirm that GABA-receptor stimulation affects acid secretion via peripheral pathways. Intravenous injection of baclofen (0.5 mg/kg), a GABAB-receptor agonist, increased acid secretion significantly from the gastric fistula and the Heidenhain pouch. These studies suggest that GABA may play a role in regulating gastric acid secretion and gastrointestinal and pancreatic endocrine function by both central and peripheral mechanisms.

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 < 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 < 0.01). Mean basal and postprandial serum gastrin concentrations were twofold to threefold higher in vagotomy patients than in controls (p < 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.