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In 23 Zollinger-Ellison patients who had been treated continuously with cimetidine for more than 3 months repeated measurements of basal acid output (BAO) were carried out 10-12 h after the last drug dose, to evaluate the prolonged inhibition of gastric acid during continuous cimetidine treatment. Most patients had a markedly prolonged inhibition of BAO after a few weeks of treatment compared with the BAO before cimetidine treatment. The prolonged inhibition became significant after 6 to 12 months of treatment (p less than 0.05). In some patients the prolonged inhibition was transient. In seven patients cimetidine therapy was discontinued for 3 days. Measurement of BAO after 12, 36, and 60 h of withdrawal revealed a marked inhibition lasting more than 60 h in four patients. Determination of plasma cimetidine could not demonstrate any detectable amounts after 12 h of withdrawal. The prolonged inhibition of BAO observed during continuous cimetidine treatment is of significant importance for evaluating secretory data. The phenomenon is still unexplained.

Changes in gastric acid secretion during the 1st year after selective gastric (SGV) and parietal cell (PCV) vagotomy for duodenal ulcer disease were studied. Pentagastrin tests were performed preoperatively and 3 months and 1 year after surgery in 383 SGV and 302 PCV patients. Resting juice pH showed after both operations a trend towards the preoperative distribution from 3 months to 1 year. Basal acid output showed a similar pattern. The initial reduction in pentagastrin-stimulated peak acid output (PAOpg) was most pronounced after SGV, but an increase occurred for both operations during the 1st postoperative year. An exception from this was the minority of patients who had a less than 20% initial reduction. They had a further decrease in their PAOpg. No sex difference and no influence of the duration of symptoms could be demonstrated. The patients with less than 20% initial reduction were younger than the other groups, and this applied for both SGV and PCV. The patterns of change in gastric acid secretion during the first year after vagotomy suggest that biologic factors are active, in addition to the effect of the surgical technique.

Ninety-one patients with duodenal, pyloric, or prepyloric ulcers were studied endoscopically. Spontaneous ulcer healing was seen in 29 patients within 2 weeks (rapid healing) and in 23 patients within 6 weeks (slow healing). More ulcers healed spontaneously in women than in men (P less than 0.05). Spontaneous healing in men was related to a low gastric peak acid output (P less than 0.05). During follow-up study for 2 years of patients with spontaneously healed ulcers 13 patients had no recurrence, whereas 19 patients had 1 or 2 recurrences, which also healed spontaneously; 11 patients had to be given active treatment, and 9 patients did not complete the study. Cigarette smoking was more frequently recorded in the group receiving active treatment than in the group with spontaneous healing. In men ulcers needing active treatment during the follow-up period were related to a high peak acid output (P less than 0.05).

Erosive prepylocic changes (EPC) is an endoscopic diagnosis based on the presence of standing prepyloric folds, with erosions (grade 3), red spots/streaks (grade 2), or without visible macroscopic lesions (grade 1). The results show that EPC is a highly reproducible finding, the endoscopic grades being interrelated. EPC grade 2 or 3 (‘active’ EPC) is shown to be associated with non-ulcer dyspepsia (NUD) and is a frequent finding at routine upper endoscopy when this is performed as a primary examination (instead of X-ray) in dyspeptic patients (1). We do not believe that EPC and ulcer are aspects of the same disease. Several observations contribute to distinguishing EPC from ulcer: Most patients have a long disease history without peptic ulcer, and the symptomatic response to cimetidine treatment is less striking than that generally found in ulcer patients. Concerning the pathogenesis of EPC, no fundamental disturbance has yet been disclosed. Maximal acid output and intragastric bile acid concentrations ar...

Increasing doses of gastrin 1-17 (G1-17) were administered to totally isolated, vascularly perfused rat stomachs prestimulated with the phosphodiesterase inhibitor isobutyl methylxanthine (IMX). Vascular and luminal histamine outputs and luminal acid output were monitored at short intervals. G1-17 induced an immediate histamine release to the vascular perfusate, preceding the increase in acid secretion by approximately 10 min. Vascular histamine output increased from a base line (IMX only) of 4.0 +/- 0.4 to a maximum of 34.5 +/- 7.3 nmol/60 min (mean +/- SEM) after 1040 pM G1-17, and acid output from 8.0 +/- 2.8 to 61.5 +/- 7.0 mumol/60 min after 520 pM G1-17. Acid output was correlated to vascular histamine release (r = 0.64, p less than 0.001). Gastrin produced a histamine release giving gastric venous concentrations of the same magnitude as the concentration of histamine necessary to induce a comparable acid response. Histamine release to the lumen, on the other hand, paralleled the acid secretion in time, suggesting it to be a passive phenomenon secondary to acid secretion. Thus, the present study for the first time shows that gastrin induces vascular histamine release of such a magnitude that this substance could be the mediator of the gastrin effect on acid secretion.

Augmented histamine tests were performed in 349 patients with duodenal ulcers verified by operation, of whom 268 were men between 16 and 84 years of age, and 81 were women between 12 and 78 years; all were citizens of Copenhagen. In the men the mean peak acid output was 44 mEq H+ per hour, ranging from 16.8 to 111.4 mEq. The mean acid output in women was 32.3 mEq H+ per hour, ranging from 13.7 to 74.4 mEq. In men with duodenal ulcer a statistically significant correlation between age and peak acid output is clearly demonstrable, the acid output decreasing by 5 mEq H+ per hour for each ten years' increase of age. In women, the acid output falls about two mEq H+ per hour per decade, although the statistical significance of this finding is not certain.

Eight studies of gastric acid secretion in a basal hour and after a single intravenous injection of soluble insulin (0.003–0.4 units/kg) were performed in a healthy man. The peak acid output after insulin was significantly correlated with the lowest concentrations of blood glucose and the maximum fall in blood glucose. Peak acid output increased linearly with log dose of insulin up to a dose of 0.05 units/kg, and higher doses evoked a smaller response. Insulin-stimulated acid secretion is dose-dependent, although the dose of insulin which produces the greatest acid output varies between individuals. Insulin hypoglycaemia produces a quantitative vagal acid response, a blood glucose of about 25 mg/100 ml is associated with the greatest acid stimulation, and blood glucose concentration below 15 mg/100 ml is associated with inhibition of acid secretion.

The effect of I.C.I. 50,123 (pentapeptide) on acid secretion in man was investigated in 36 patients. It is presumed that continuous intravenous infusion of I.C.I. 50,123 (pentapeptide) in a dose of 0.1 μg/kg/minute produces maximal acid output. Administration of a larger dose sometimes causes decrease in acid production. I.C.I. 50,123 (pentapeptide) administered intravenously in a dose of 0.1 μg/kg/minute produces approximately the same acid output as does histamine given intravenously in a dose of 0.7 μg/kg/minute. In most cases maximal acid output after infusion of I.C.I. 50,123 (pentapeptide) occurs in the second 15-minute period. After histamine maximal acid output is attained a little later—in the third or fourth 15-minute period. Side-effects after intravenous administration of I.C.I. 50,123 (pentapeptide) were in only one case of such severity that the test had to be broken off. It is concluded that I.C.I. 50,123 (pentapeptide) given intravenously in a dose of 0.1 μg/kg/minute is adequate for evalu...

Volume, pH, and total acidity of the basal and of the stimulated gastric secretion were measured in guinea-pigs before, and at appropriate intervals after, x-irradiation to the stomach area. A great reduction of the stimulated acidity and acid output was found. It reached a maximum between the second and the fourth week after irradiation. Thereafter the total acidity increased gradually, but, 56 weeks after irradiation, it still remained significantly below the normal (p < 0.05). The volume was lowered to a lesser extent.

In a correlative study the gastric acid output and cyclic 3′, 5′-adenosinc monophosphate contents of gastric mucosa were determined in rats. With respect to sex no significant differences were obtained. A concomitant diurnal rhythm was demonstrated for both acid output and cyclic AMP contents of gastric mucosa characterized by a peak at midnight and a trough at noon.

The pentagastrin-stimulated gastric volume and acid output were measured with and without an i.v. thyrotropin-releasing hormone (TRH) infusion (666 microgram/h). TRH inhibited the pentagastrin (6 microgram/kg s.c.) stimulated volume to 67.5 +/- 8.4% (p less than 0.01) and the acid output to 65 +/- 8.4% of control infusion values (mean +/- S.E.M.). It is concluded that TRH inhibits the pentagastrin-stimulated gastric secretion in man.

Recent studies suggest a normal maximum acid secretion in duodenal ulcer patients with a history of less than three years, but an increase of secretion in those with longer history. The validity of this hypothesis was investigated in groups of patients with operatively verified duodenal ulcer and history for less than 3, 3--6, and 7--10 years. Each group, including 21 men and nine women, was compared to two male and one female group of age-matched controls without dyspepsia. In smaller groups of 16 men it was possible to compare age-matched groups from a population of 376 men with histories for up to 22 years. Finally, 11 men with an ulcer history of less than one year were compared to 11 controls. All subjects had measurements of MAO by the augmented histamine test. MAO was significantly higher in patients with a history less than one year and less than three years, respectively, compared to controls. After correction of MAO for weight or lean body mass the difference remained significant in men, but not in the smaller groups of women. MAO in men with a history of from less than three up to 22 years did not show any maximum. Thus, the study did not support the assumption that gastric hypersecretion is a result of duodenal ulceration.

The ‘basal’ gastric secretion collected during 3 hours with a gastric Levin tube and a gastroduodenal Lagerlof tube was compared in 11 subjects. The Lagerlof tube gave significantly higher pepsin output, pepsin concentration, and pepsin/acid ratio than the Levin tube, and showed a significant non-steady state level of volume, acid concentration, acid output, pepsin output, and pepsin/acid ratio. The effect of the Lagerlof tube was not dependent on the duodenal drainage. Perfusing the duodenum with secretin-stimulated duodenal juice in 4 subjects did not stimulate more pepsin than the tube alone.

Follow-up studies were made of 14 congenital pyloric stenosis patients between 21 and 27 years after Fredet-Ramstedt pylorotomy. Minor dyspeptic discomfort was common, but only two had symptoms of any severity. Acid secretion studies showed generally high fasting and basal secretion, both acid and volume. Following pentapeptide stimulation, volume secretion was about 40% higher than in normal individuals, but peak acid output was within normal limits. Barium meal studies showed no gastric, pyloric or duodenal abnormality. Two patients had retention. No patient had symptoms of dumping.

Dose-response (DR) curves for acid output to histamine and pentagastrin were determined by two techniques in conscious cats with gastric fistulas With the continuous DR technique, the dose of the stimulant was doubled each hour; with the single DR technique, only one dose of the stimulant was infused on each test day. The DR curves for histamine did not differ with the two techniques; for pentagastrin, the acid responses were higher with the single DR than with the continuous DR technique. For both histamine and pentagastrin, the dose for half the maximal response did not differ with the two techniques. The DR curves were also analysed by application of the Michaelis-Menten equation.

In 18 children, 9–30 months of age, without gastrointestinal disorders, the gastric secretion of pepsin was studied before and after augmented histamine stimulation.Histamine resulted in a slight increase of the hourly pepsin output, which, however, was not significantly higher than in the basal hour. The basal pepsin output was significantly correlated to age and body surface area, while the stimulated pepsin output was not significantly correlated to age, body-weight, body surface area, basal pepsin output, or stimulated acid output.