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.     

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.     

Pancreatic polypeptide response to insulin in duodenal ulcer. Different levels in accordance with ulcer activity and its response to treatment

Pancreatic polypeptide is said to be a marker of vagal tone in duodenal ulcer. To determine whether pancreatic polypeptide levels are related to the course of duodenal ulcer, we studied acid and pancreatic polypeptide responses to insulin in 80 patients with duodenal ulcer disease: 40 with unoperated duodenal ulcer and 40 with proximal vagotomy. Data were analysed in accordance with the presence of an ulcer (active disease) and, when present, in accordance with the ulcer healing on medical treatment (cimetidine, 1 g/day for 4 weeks). In both groups acid and pancreatic polypeptide responses to hypoglycaemia were slightly correlated (r = 0.38) (p less than 0.05). The basal pancreatic polypeptide level was higher in patients with active disease than in those with inactive disease, who had a basal level similar to that of normal subjects of the same age range. Like the insulin-stimulated acid secretion, the pancreatic polypeptide response to insulin hypoglycaemia was higher in patients with active disease than in those with inactive disease (p less than 0.05): 26.1 +/- 3.9 versus 20.1 +/- 4 nmol/l/120 min, respectively, in unoperated patients and 34.8 +/- 2.2 versus 24.3 +/- 2.5 nmol/l/120 min, respectively, after proximal vagotomy. In active disease the pancreatic polypeptide response to insulin hypoglycaemia was higher in subjects whose ulcer did not heal further after cimetidine therapy than in those whose ulcer did. These data suggest that the pancreatic polypeptide response to insulin is an indicator of duodenal ulcer activity and is related to the treatment efficacy. These relationships are partly mediated by increased vagal tone.     

Comparison of the effects of ranitidine, cimetidine and placebo on the 24 hour intragastric acidity and nocturnal acid secretion in patients with duodenal ulcer.

Twenty-four hour intragastric acidity and nocturnal acid secretion were measured in 10 males with duodenal ulcer in four separate 24 hour studies, during which the subjects ate normal meals, had unrestricted physical activity, and consumed their customary quantities of tobacco. The medication consisted of either placebo, cimetidine 200 mg tds and 400 mg at night, or ranitidine 150 mg bd, or 200 mg bd. Ranitidine 150 mg bd decreased mean 24 hour hydrogen ion activity from 41.8 mmol/l to 13.1 mmol/l (-69%, P less than 0.001) and nocturnal acid output from 6.1 mmol/h to 0.6 mmol/h (-90%, P less than 0.01). This degree of inhibition was significantly greater than that due to cimetidine (P less than 0.001 for 24 hours acidity, less than 0.05 for night time acid output). Plasma concentrations of ranitidine were greater than the IC50 for more than eight hours after the 150 mg dose. Ranitidine 200 mg conferred no additional advantage. Ranitidine 150 mg bd should be tested in therapeutic trials.     

Effect of cimetidine on gastric secretion and duodenogastric reflux.

In 19 subjects (four controls, one gastric ulcer and 14 duodenal ulcer) maximal gastric secretion was evoked with histamine 0.13 mumol/kg/h (0.04 mg/kg/h) for two to two and a half hours. A slow intravenous bolus dose of 200 mg cimetidine was given at the beginning of the last hour. Gastric secretion was measured before and after cimetidine administration and expressed both as mean acid output (mmol H+/h) and 'pyloric loss and duodenogastric reflux corrected' volume (Vg, ml/h). Mean reduction by acid output was 86%; mean reduction by corrected volume (Vg) was only 64%. The discrepancy, which is significant (p less than 0.01), is caused by a marked increase in duodenogastric reflux after cimetidine.     

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.     

Simultaneous measurement of gastric acid and duodenal alkali secretion by in situ titration in health and disease.

We have devised a technique for simultaneously measuring the acid secretion into the stomach and alkali into the duodenum by in situ titration using a modification of the technique of Fordtran and Walsh. Using this technique, the results of acid and alkali secretion measured simultaneously were identical with those obtained using the conventional aspiration method on separate days. In response to stimulation with pentagastrin acid output was 17.2 +/- 1.4 vs 15.4 +/- 1.9 mmol/h and alkali response with secretin was 16.0 +/- 0.8 vs 14.4 +/- 1.5 mmol/h. The response to food was measured in 10 control subjects, 10 patients with duodenal ulcer, and 10 patients with pancreatitis. In controls, the acid and alkaline secretion were similar (15.8 +/- 1.7 vs 18.2 +/- 1.3 mmol/h), in patients with duodenal ulcer acid secretion was significantly greater than alkaline secretion (31.9 +/- 2.2 vs 21.9 +/- 1.7 mmol/h), and in patients with pancreatitis the alkali secretion was significantly less than acid (19.8 +/- 1.9 mmol/h acid vs 11.4 +/- 0.6 mmol/h alkali). It can, therefore, be concluded that in response to food the patients with duodenal ulcer are significant hypersecretors of acid (DU acid greater than DU alkali output) and patients with pancreatitis are significant hyposecretors of alkali (pancreatitis-alkaline output less than acid output) and normal subjects secrete equal amounts of acid and alkali.     

Effects of transdermal scopolamine, alone or in combination with cimetidine, on total 24 hour gastric acid secretion in patients with duodenal ulcer.

Transdermal scopolamine is an antimuscarinic preparation approved for use in the United States for prevention of motion sickness. A recent study using this drug (0.5 mg/patch) suggested that enough scopolamine was absorbed through the skin to reduce basal gastric acid secretion in patients with duodenal ulcer. We have compared the effect of transdermal scopolamine and oral cimetidine (400 mg twice daily) in seven men with chronic duodenal ulcer, both alone and in combination, on acid secretion throughout an entire 24 hour period in a placebo-controlled, randomised, double blinded cross over study. The effect of these drugs on basal, interprandial, and nocturnal gastric juice volume and hydrogen ion concentration also was measured. Transdermal scopolamine had no significant effect on mean 24 hour acid secretion (placebo, 409.4 mmol/day; scopolamine, 364.0 mmol/day) nor did it have a significant effect on gastric juice volume or hydrogen ion concentration. The combination of transdermal scopolamine plus cimetidine was not more effective than cimetidine alone in reducing total 24 hour acid secretion (mean, 231.8 versus 235.3 mmol/day) nor in reducing gastric juice volume or hydrogen ion concentration.     

Gastric acid and pancreatic polypeptide responses to modified sham feeding. Effects of truncal and parietal cell vagotomy.

The effects of truncal vagotomy and parietal cell vagotomy on gastric acid secretion and plasma gastrin and pancreatic polypeptide release were studied in 28 duodenal ulcer patients under basal conditions and after modified sham feeding and infusion of pentagastrin (2 micrograms/kg/h). Before vagotomy gastric acid output in response to modified sham feeding was significantly higher than basal acid secretion in all subjects tested and reached about 45% of the pentagastrin maximum. No difference in the increase in acid response, or in the pancreatic polypeptide response to modified sham feeding was found between patients with high and low basal secretion. Plasma gastrin concentration was unaltered by modified sham feeding before and after truncal vagotomy or parietal cell vagotomy, although after vagotomy it tended to reach higher values than before this procedure. After truncal vagotomy, basal pancreatic polypeptide concentration was decreased and modified sham feeding-induced pancreatic polypeptide increment was completely eliminated. Four weeks after parietal cell vagotomy, the modified sham feeding-induced increment in plasma pancreatic polypeptide was significantly decreased and observed only in seven of 12 patients. Four to five years after parietal cell vagotomy all subjects responded to modified sham feeding with pancreatic polypeptide increment similar to that before vagotomy and in three of 12 patients acid response to modified sham feeding was seen. This study indicates that truncal vagotomy eliminates gastric acid and plasma pancreatic polypeptide responses to vagal excitation while parietal cell vagotomy abolishes gastric acid response and reduces temporarily the pancreatic polypeptide response to modified sham feeding (possibly because of transient impairment of the vagal innervation of the pancreas). (2) A high ratio of basal to maximal acid output in non-operated duodenal ulcer patients is not associated with a low acid response to modified sham feeding, nor with a high pancreatic polypeptide concentration, and (3) Restitution of the pancreatic polypeptide response to modified sham feeding five years after parietal cell vagotomy does not indication ineffective denervation of the parietal cells.     

Single evening administration of etintidine in the human: effect on acid secretion and behavior of important hormones

The potency and duration of action of a single dose of etintidine, ranitidine and cimetidine were compared in placebo-controlled studies. In addition, the effect of a single night-time dose of etintidine (600 mg) on gastric acid secretion and basal hormone levels was assessed before, during and after a 28-day treatment. Nocturnal gastric acidity (23.00-07.00) was inhibited from 41.04 +/- 5.0 mmol/l to 12.9 +/- 2.8 mmol/l by 300 mg etintidine, to 6.50 +/- 2.5 mmol/l by 600 mg etintidine and to 8.58 +/- 2.5 mmol/l by 800 mg cimetidine nocte. Etintidine and cimetidine did not reduce H+-concentrations during the following day. Pentagastrin-stimulated acid output was virtually not affected after 600 mg etintidine and 800 mg cimetidine as well. By contrast, stimulated acid secretion was still suppressed by about 50% following 300 mg ranitidine. Basal levels of testosterone, prolactin etc. remained unchanged by 28-day etintidine (600 mg dose at night) treatment. Clinical studies are needed to examine the place of the single dose of etintidine (600 mg) at night for the short-term treatment of duodenal ulcer.     

Physiopathological Heterogeneity of the Duodenal Mechanisms that Inhibit Gastric Acid Secretion in Duodenal Ulcer Patients

The effect of duodenal acidification on pentagastrin-stimulated gastric acid secretion was studied in 43 duodenal ulcer patients and in 17 normal controls. Three types of responses were observed: group A, no inhibition of gastric acid secretion occurred in 17 (40%) ulcer patients and in three (18%) controls (p less than 0.05); group B, inhibition of gastric acidity occurred in seven (16%) ulcer patients and in 12 (71%) controls (p less than 0.05), and group C, retarded gastric acid inhibition occurred in 19 (44%) duodenal ulcer patients and in 2 (12%) controls (p less than 0.05). Secretin levels did not increase after duodenal acidification, the higher percentages of failure being observed in groups A and C (p less than 0.05). The pH of the duodenal aspirate was 4.9 +/- 2 and 7.7 +/- 1.4 in ulcer patients and controls, respectively (p less than 0.05), with the low levels being detected in groups A and C (4.7 +/- 2 and 5.3 +/- 2.1) compared to group B (7.3 +/- 1.7; p less than 0.05). The results show that responses of duodenal ulcer patients to duodenal acidification are heterogeneous, and that failure of gastric secretion inhibition and defective intraduodenal acid neutralization are related.     

Effects of single daily doses of a pyridil-2-tetrahydrothiophene derivative (40749 RP) on 24 hour H+ activity, nocturnal acid output, gastrin and pepsinogen I profiles in duodenal ulcer patients

40749 RP is a pyridil-2-tetrahydrothiophene derivative, belonging to a new class of gastric antisecretory drugs. We compared its effects on gastric secretion with cimetidine. Intragastric acidity, nocturnal acid output, gastrin and pepsinogen-I profiles were measured in patients with duodenal ulcer in clinical remission. A single dose of 100 mg 40749 RP reduced median 24 h gastric acidity as effectively as cimetidine 1000 mg given as four divided doses, 0.63 vs 1.6 mmol/l. Continued treatment with 40749 RP for 10 days reduced the median 24 h gastric acidity even further, to 0.006 mmol/l (p less than 0.001) and significantly increased fasting concentrations of gastrin and pepsinogen-I (p = 0.02). The incremental gastrin secretion to a standard meal was significantly increased after 10 days treatment with 40749 RP when compared with the first day of 40749 RP, or with cimetidine. These results show that 40749 RP exerts a powerful inhibitory effect on gastric acid secretion after a single 100 mg dose, and that this inhibitory effect increases with continued administration.     

Comparison of an intragastric method of estimating acid output with the pentagastrin test in normal and duodenal ulcer subjects.

Using Fordtran's technique but substituting the meat extract Oxo for the steak meal we investigated gastric acid secretion in eight control subjects and nine patients with chronic duodenal ulcer. Intragastric titration was performed using a double lumen tube measuring the pH in the stomach every three minutes and adjusting it to 5.5 throughout the test by infusing 0.3-M sodium bicarbonate. On a separate day a pentagastrin test was performed using a conventional gastric aspiration technique. In the eight control subjects the mean acid output after pentagastrin was 13.7 +/- 2.1 (SEM) mmol/h, whereas the mean hourly acid output measured by intragastric titration was 20.1 +/- 3.1. The greater response to Oxo than to pentagastrin in the controls (deltaAO = + 46%) was significant (P less than 0.01). This is in contrast with our duodenal ulcer patients whose mean hourly acid outputs were 22.7 +/- 4.4 and 23.0 +/- 4.4 mmol/h in response to pentagastrin and Oxo respectively (r = 0.95). The findings, while clearly at variance with those of Fordtran and Walsh (1973), are more in keeping with the concept of increased endogenous secretory drive in duodenal ulcer patients compared to normal subjects.     

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)     

Effect of proximal gastric vagotomy on the competence of the lower sphincter of the esophagus

The aim of this prospective study was to assess the effects of highly selective vagotomy on lower esophageal sphincter pressure, and to determine whether or not it leads to increased gastroesophageal reflux. Fifteen patients (4 females, 11 males), mean age 43 years (22-63) suffering from duodenal ulcer without any clinical or pH evidence of gastroesophageal reflux were treated by highly selective vagotomy. All of them were studied before and 3-6 months after operation by history taking, pH reflux, manometric, and acid secretory pentagastrin tests. After operation none of the 15 patients had clinical evidence of duodenal ulcer or gastroesophageal reflux. The basal and stimulated acid outputs were decreased after vagotomy; pre and postoperative values were 6.8 +/- 8.9 mmol/h and 0.9 +/- 1.6 mmol/h; 42.2 +/- 10.3 mmol/h and 21.4 +/- 6.4 mmol/h, for BAO and PAO respectively (p less than 0.001). The lower esophageal sphincter pressure was 22.5 +/- 5.6 cm H20 before and 21.1 +/- 4.9 cm H20 after surgery (p less than 0.01). None of the values were lower than normal. There was no significant difference in pH reflux tests; the total duration of pH less than 5 reflux was 1.2 +/- 2.1 p. 100 before, and 1.9 +/- 2.8 p. 100 after vagotomy. These results suggest that an efficient highly selective vagotomy does not impair lower esophageal sphincter efficiency in patients-without gastroesophageal reflux, and that the routine addition of an antireflux procedure is not well advised.     

Lithium fluxes across the gastric mucosa after truncal vagotomy and drainage--an objective assessment of mucosal injury.

Gastric mucosal permeability to lithium has been measured in 20 patients with an untreated duodenal ulcer, eight patients who were asymptomatic for more than one year after truncal vagotomy and drainage, 14 patients with an endoscopically proven recurrent ulcer, and 21 patients with an unsatisfactory result from truncal vagotomy and drainage for other reasons. Lithium fluxes were lowest in the asymptomatic postoperative patients (0.149 +/- 0.028 mmol Li+/15 min), but were not significantly different to the measured fluxes in patients with a duodenal ulcer before treatment (0.160 +/- 0.020 mmol Li+/15 min) or a recurrent ulcer after truncal vagotomy and drainage (0.169 +/- 0.022 mmol Li+/15 min) (SEM). By comparison the mean lithium flux in patients who were dissatisfied with the results of their previous surgery for reasons other than a recurrent ulcer (0.234 +/- 0.019 mmol Li+/15 min) was significantly higher than that observed in patients with a duodenal ulcer (p less than 0.05), patients with a recurrent ulcer (p less than 0.05) or patients who were asymptomatic after definitive ulcer surgery (p less than 0.02). Furthermore, when the lithium fluxes observed in 11 patients whose major postoperative complaint was bile vomiting (0.243 +/- 0.027 mmol Li+/15 min) were compared with results from the remaining 52 patients included in the study (0.173 +/- 0.012 mmol Li+/15 min) fluxes were significantly higher in the 'bile vomiters' (p less than 0.05).     

Effect of cimetidine on the amounts of histamine in the gastric mucosa of patients with gastric or duodenal ulcers.

Measurements were made of the amounts of histamine extracted from patients with peptic ulcer disease and control subjects suffering from various gastrointestinal diseases. Patients with duodenal ulcer, gastric ulcer, or recurrent duodenal ulcer after proximal gastric vagotomy often had less gastric mucosal histamine than did normal controls. Cimetidine therapy increased the amounts of the histamine to above control levels, presumably by suppression of output. It is concluded that endogenous amounts of histamine reflect the pathogenic states in the gastric mucosa of patients with peptic ulcer diseases. Cimetidine, as does vagotomy, increases the amount of gastric mucosal histamine. These findings suggest that the increase in mucosal histamine with cimetidine is not due to activation of histamine methyl transferase, but rather to suppression of histamine output into the gastric juice.     

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, prepyloric, and combined duodenal/prepyloric ulcer disease: three distinct entities of juxtapyloric ulcer disease?

One hundred and seven patients with long-standing and severe chronic juxtapyloric ulcer disease were classified in accordance with the location of the present ulcer and previous ulcers into 1) pure duodenal (DU), 2) pure prepyloric (PU), and 3) combined duodenal/prepyloric (DU/PU) or prepyloric/duodenal (PU/DU) ulcer disease. In a prospective follow-up study over a 3-year period after parietal cell vagotomy (n = 39) or during continuous treatment with cimetidine (n = 62) patients with DU had recurrent ulcers located exclusively to the duodenal bulb and patients with PU, exclusively to the prepyloric region. In patients with DU/PU and PU/DU recurrent ulcers occurred on either side of the pylorus. Basal acid and basal pepsin outputs were higher and bile acid in gastric juice was lower in patients with DU than in those with PU. There are a considerable number of patients who possess features of both duodenal and prepyloric ulcer disease. The clinical outcome of both continuous cimetidine treatment and vagotomy in these patients (DU/PU and PU/DU) was less satisfactory than in pure DU. All patients presenting with active DU should therefore be investigated for evidence of previous prepyloric ulceration.     

Gastric acid secretion and its predictive value after vagotomy for perforated duodenal ulcer

In a prospective randomized clinical trial, gastric acid secretion was compared in patients after simple closure, proximal gastric vagotomy with closure, or truncal vagotomy with pyloroplasty performed for perforated duodenal ulcer. The basal and pentagastrin- and insulin-stimulated acid outputs were similar after either proximal gastric or truncal vagotomy; they were also comparable with the postoperative acid values after corresponding procedures performed electively for chronic duodenal ulcer. Conversely, the basal and maximum acid outputs after simple closure of perforation were no different from the preoperative acid outputs of a group of duodenal ulcer patients matched for age and sex. The efficacy of acid reduction by emergency proximal gastric and truncal vagotomy was shown by the respective ulcer recurrence rate of 3% (1/34) and 6% (2/32) compared with 43% (15/35) after simple closure (p less than 0.01). Acid secretory data and serum gastrin levels did not predict ulcer relapse in patients after simple closure of perforation.