SUMMARY Gastric acid and serum gastrin, pancreatic polypeptide, and insulin responses to cephalic vagal stimulation were studied in eight patients with duodenal ulcer using modified shamfeeding for periods varying from four to 30 minutes. In addition, the maximal acid response to sham-feeding was compared with that induced by pentagastrin in 10 healthy subjects and 14 patients with duodenal ulcer. It was found that the gastric acid response to modified sham-feeding reached the maximal value after 15 minutes of sham-feeding and amounted to about 68% of the pentagastrin maximum. The serum pancreatic polypeptide response was also increased after modified sham-feeding and depended on the duration of this procedure, whereas gastrin and insulin responses were not significantly affected by modified sham-feeding. When the peak acid output induced by modified sham-feeding was normalised as percentage of the peak response to pentagastrin, it was similar in healthy subjects and in patients with duodenal ulcer; this indicates that the increased peak acid response to modified sham-feeding observed in patients with duodenal ulcer corresponded with their greater parietal cell mass rather than with increased vagal tone.It is well established that the physiological vagal excitation accomplished by the 'chew and spit' technique results in a potent gastric secretory stimulation1 3 accompanied by a rise in plasma hormonal levels.3 7 The gastric acid secretory rate achieved by this modified sham feeding in duodenal ulcer patients was found to be of similar range to that attained by adequate sham-feeding,8 but no study was performed to determine the relationship between the duration of the modified sham-feeding and the gastric secretory response. In dogs, it has been shown that a marked gastric secretion occurred after less than one minute of sham-feeding and that when the duration of sham-feeding was extended there was a further increase in gastric secretion9 and proportional increments in plasma gastrin or insulin levels were observed.5 The maximal acid response to shamfeeding in these animals was not significantly different from that achieved by gastrin.9 No similar studies have been so far performed in man, although the modified sham-feeding has been widely used to study vagal control of gastric secretion.*Address for correspondence: Professor Dr SJ Konturek, Institute of Physiology, 31-531 Krak6w, ul. Grzegorzecka 16, Poland.Received for publication 16 May 1981 This study was designed to determine the relationship between the duration of the modified sham-feeding and the gastric secretory and plasma hormonal responses to this procedure and to compare the maximal gastric acid response to modified sham-feeding and to pentagastrin in healthy subjects and duodenal ulcer patients. Methods SUBJECTSTen healthy male subjects (mean age 20 years, range 19-22 years; mean weight 71 kg, range 66-77 g) and 20 male patients (age 20 years, range 19-23 years; mean weight 68 kg, range 61-75 kg) with wellestablished chronic duodenal ulcer disea...

This study was designed to determine the specificity and physiological nature of short-term satiety effects of cholecystokinin (CCK) in rats with intact and transected vagal nerves. Rats with-the gastric fistulas, closed or open, were used for normal feeding or sham feeding of liquid meal offered for 30 min. CCK-8 (0.5-10 nmol/kg) injected intraperitoneally (ip) 15 min before feeding inhibited food intake dose dependently in both normal-fed and sham-fed rats at a minimal inhibitory dose of 1 nmol/kg. CCK-8 at the same doses caused a potent stimulation of pancreatic protein secretion, reaching maximum at a dose of approximately 0.5 nmol/kg. Pretreatment with a potent CCK receptor antagonist, L-364,718 (2.5 mg/kg ip), increased food intake during normal feeding (but not sham feeding) and almost completely blocked the satiety and pancreatic stimulatory effects of CCK. When feeding was preceded by intragastric administration of proteinase inhibitor (Foy-305, 200 mg/kg), food preload, or diversion of bile-pancreatic secretion to the exterior, there was a significant increase in the plasma level of CCK and an inhibition of food intake by about 36, 78, and 25%, respectively. Pretreatment with L-364,718 completely abolished this inhibition by Foy-305 and bile-pancreatic diversion and reduced that caused by food preload. Among other gut peptides given ip (10 nmol/kg) only bombesin reduced food intake, whereas gastrin, secretin, gastric inhibitory polypeptide (GIP), pancreatic polypeptide (PP), and peptide YY (PYY) were ineffective.(ABSTRACT TRUNCATED AT 250 WORDS)

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.