SUMMARY The effects of ranitidine, a new H2-receptor antagonist which does not contain an imidazole ring, and cimetidine have been determined on histamine, meal-induced gastric acid secretion, and serum gastrin levels in duodenal ulcer patients. Compared with cimetidine, ranitidine was found to be about eight times more potent an inhibitor of histamine-induced secretion and four to five times more potent an inhibitor of sham-feeding, effecting serum gastrin levels.The discovery by Black and his associates' of a new class of drugs that specifically block the action of histamine on gastric acid secretion has revolutionised the treatment of peptic ulcer and other acid-pepsin diseases. The beneficial effects of these so-called H2-receptor antagonists on ulcer healing and symptom relief result from their potent inhibitory action on gastric acid secretion induced not only by histamine but also by a variety of other stimulants including gastrin, acetylcholine, stable cholinergic esters, caffeine, insulin, gastric distention, shamfeeding, and real feeding.23At present, cimetidine (Tagamet) is the only widely accepted representative of this type of agent which blocks H2-receptors, an action thought to be due to the imidazole ring present in its structure.4 Recently, a new compound, ranitidine, has been shown to block H2-receptors in the stomach of laboratory animals5 and in man.6 7 but this compound does not have an imidazole ring. Thus a study was undertaken to compare the effectiveness of ranitidine and cimetidine in inhibiting histamine and sham-feeding or meal-induced gastric secretion in duodenal ulcer patients. MethodsThe study group consisted of 12 patients with wellestablished chronic duodenal ulcer (DU) disease and a mean age of 22 years (range 20-25 years) and mean

The effect of somatostatin, a growth hormone releasing-inhibiting hormone (GH-RIH) on basal and meal-, pentagastrin-, or histamine-stimulated gastric acid and pepsin secretion was studied in six duodenal ulcer patients. Intravenous GH-RIH infused in graded doses ranging from 0.62 to 5.0 microgram/kg/hr produced a dose-related inhibition of pentagastrin-induced acid secretion reaching about 15% of control level at the dose of 5.0 microgram/kg/hr. Acid inhibition was paralleled by a decrease in the pepsin output and accompanied by a dose-dependent reduction in serum growth hormone and insulin levels measured by radioimmunoassay. GH-RIH used in a single dose of 2.5 microgram/kg/hr produced about 85% inhibition of acid secretion induced by a meal (measured by intragastric titration) accompanied by a significant decrease in serum gastrin and insulin levels. The effect of GH-RIH on histamine-stimulated secretion was very modest and observed only after stopping the GH-RIH infusion. Thus GH-RIH suppressed acid and pepsin secretion induced by pentagastrin and a meal, and this effect was accompanied by a suppression of serum growth hormone and gastrin levels which may contribute to the inhibition of gastric secretion observed.

SUMMARY In 10 healthy subjects and 25 duodenal ulcer patients, gastric acid and pepsin and serum gastrin responses to cephalic-vagal stimulation induced by modified sham-feeding (MSF) were studied before and after vagotomy and atropinisation and compared with those to maximal stimulation with pentagastrin. When the MSF-induced peak acid output was normalised as a percentage of peak response to pentagastrin it was about 62 % in healthy subjects and 66 % in duodenal ulcer patients. Serum gastrin concentration was not changed significantly by modified sham-feeding either in normal subjects or in duodenal ulcer patients. Truncal vagotomy completely abolished gastric acid and pepsin responses to MSF in duodenal ulcer patients. Atropine almost completely suppressed gastric acid and pepsin responses to MSF in healthy subjects and reduced those in duodenal ulcer patients by about 62 %. The combination of the modified sham-feeding and pentagastrin infusion resulted in augmentation of the acid output in duodenal ulcer patients but not in healthy subjects. This study shows that the cephalic phase results in a potent gastric acid and pepsin stimulation which is not accompanied by any change in serum gastrin concentration either in healthy subjects or duodenal ulcer patients and which is abolished by vagotomy and suppressed by atropine.Physiological vagal excitation accomplished by the 'chew and spit' method was reported to induce a potent gastric secretory stimulation which was shown to be of similar magnitude to that attained by a real sham feeding technique (Stenquist et al., 1976 stimulation of gastric secretion in healthy subjects and duodenal ulcer patients; (2) to examine the role of the vagal innervation and gastrin in gastric response to modified sham-feeding; (3) to measure the extent to which cephalic stimulation affects the gastric secretion induced by pentagastrin. MethodsTen healthy male subjects (mean age 20 years, range 19-22 years; mean weight 68 kg, range 64-73 kg) and 25 male patients (mean age 21 years, range 19-24 years; mean weight 66 kg, range 62-78 kg) with wellestablished chronic duodenal ulcer disease were repeatedly examined. Ten of these patients were in clinical remission when their study period began; 10 others who had typical duodenal ulcer symptoms were examined before and after truncal vagotomy and pyloroplasty. The study was approved by a Human Research Review Committee and informed consent was obtained from each subject. The patients received no anticholinergics or H2-blockers for at least five days before the secretory studies were started. 875 on 12 May 2018 by guest. Protected by copyright.

SUMMARY The ability of an amino acid mixture given intraduodenally or intravenously to stimulate gastric secretion is compared in healthy subjects and in duodenal ulcer patients. Graded amounts of amino acids by both routes produced a similar increase in acid output in healthy subjects, reaching about 30% of the maximal response to pentagastrin. Serum gastrin concentrations remained virtually unchanged but serum alpha amino acid nitrogen levels were about twice as high with intravenous as with intraduodenal administration. Intravenously administered amino acids produced a significantly higher acid output in patients with duodenal ulcer than in healthy subjects, but did not produce a significant increase in gastric acid or pepsin secretion when combined with a pentagastrin infusion as compared with pentagastrin alone. Cimetidine (2 mg/kg/h) added to intravenous amino acid infusions caused almost complete suppression of acid secretion. This study indicates that amino acids are capable of stimulating gastric secretion after intraduodenal and after intravenous administration. The response to the latter is significantly higher in patients with duodenal ulcer than in healthy subjects, does not appear to involve gastrin release, is not affected by pentagastrin, and is strongly suppressed by histamine H2-blocker.Previous studies have shown conclusively that the only known chemicals in food that stimulate gastric secretion are products of protein digestion, peptides and amino acids. The stimulation of gastric secretion by peptic digests has been attributed to the release of gastrin from the antral and intestinal G cells (Strunz et al., 1977) and to a direct action on the oxyntic glands . Unexpectedly, it has been reported recently that an amino acid mixture may stimulate gastric secretion after intravenous administration, without mediation of gastrointestinal hormones Landor and Elpidio, 1977;Landor and Ipapo, 1977).In this report, the effect of an amino acid mixture given intraduodenally on gastric acid secretion has been compared to that evoked by intravenous amino acids in patients with duodenal ulcer and in healthy subjects. ' Intraduodenal infusions were given via a double lumen gastroduodenal tube modified with two balloons. A few hours after being passed the tip was positioned at the junction of the third and fourth parts of the duodenum under fluoroscopic control and the balloons straddling the pylorus were inflated with 20 ml of air to prevent duodenogastric reflux. This caused no sensation or discomfort. The duodenal lumen was used to instill the test solution into the duodenum and the gastric lumen to aspirate gastric content (Konturek et al.,

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