Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Gastric acid responses to the test meals were measured in the Heidenhain pouch, gastric and pancreatic fistula dogs, using the intragastric titration method, and monitoring the rate at which a solution of 1-0 N-NaOH had to be added to maintain the pH of the gastric content constant at pre-selected values ranging from 5-0 to 1-0. In this way the pH profile of the gastric acid and pepsin responses to a liver extract meal kept in the Heidenhain pouch or gastric fistula as well as to exogenous stimuli such as histamine, pentagastrin or Urecholine could be determined. 2. A liver extract meal adjusted to pH 5-0 produced a potent and pressure-related stimulation of acid secretion from the Heidenhain pouch without any change in secretion from the main stomach and pancreas or in the serum concentration of immuno-assayable gastrin. 3. Graded decrease of the liver extract meal pH to below 5-0 resulted in the pH-dependent inhibition of gastric acid output, which at pH 1-0 was only about 30% of the value attained at pH 5-0. Acid secretion from the Heidenhain pouch induced by exogenous stimuli such as histamine, pentagastrin or Urecholine also showed gradual decrease when the pH of the pouch content was decreased in sequential order from 5-0 to 1-0. This pH-dependent inhibition was accompanied by an increase in pepsin secretion. 4. The pH-dependent inhibition of the Heidenhain pouch response to the liver extract meal was not altered by topical application of a local anaesthetic and atropine or by the intravenous infusion of large doses of atropine, secretin or metiamide, which were shown to cause a marked inhibition of the main stomach response to the liver meal. 5. The results indicate that there is a local and gastrin-independent inhibition mechanism of gastric acid secretion activated by an acidified meal making contact with the oxyntic gland area.
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PMID:Characteristics of gastric inhibition by acidification of oxyntic gland area. 0 Apr 91

Metiamide an histamine H2-receptors antagonist has been used to treat a case of Zollinger-Ellison syndrome characterized by a long standing diarrhea, an important gastric hypersecretion and a moderatly elevated plasma gastrin but without digestive ulceration. At the dose of 600 mg per day, Metiamide induced a complete suppression of acid secretion, an effect which lasted for 15 days after stopping the drug. Accordingly and since the only finding at time of laparotomy was a small lymph node enlarged with endocrine metastatic tissue, the stomach was left intact and Metiamide pursued. During the first 4 months of chronic administration of Metiamide, acid secretion was maintained at levels below 25 p.cent of initial values. Ulteriorly however, although dosages of Metiamide were increased, acid hypersecretion resumed and a duodenal ulcer developed. Total gastrectomy was then performed 11 months after the beginning of Metiamide. In spite of the failure of Metiamide treatment, the long term follow up of this case of Zollinger-Ellison Syndrome, allowed us to get theoretical and practical informations.
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PMID:[Zollinger-Ellison syndrome treated medically by an inhibitor of H2 histamine receptors]. 0 Jun 53

This study was undertaken to compare the ability of L- and D-isomers of amino acids bathing the oxyntic gland area to stimulate acid secretion in conscious dogs with Heidenhain pouch (HP), gastric fistula (GF) and pancreatic fistula (PF). Acid outputs from HP were determined by an intragastric titration method when amino acid solutions were perfused into HP at various concentrations, pH values, and distention pressures. Only L-isomers of all natural amino acids were found to stimulate acid secretion, whereas D-isomers of amino acids tested were completely inert in this respect. The comparison of the secretagogue activity of amino acids shows that L-histidine among essential amino acids and glycine among nonessential amino acids exhibited the strongest stimulation of acid outputs, reaching, respectively, 52 and 40% of the maximal response to histamine. Decreasing the pH of L-histidine solution perfused into HP in sequential order from 5.0 to 1.0 resulted in a stepwise reduction of acid output, falling at pH 1.0 to about 40% of the peak response achieved at pH 5.0. Local irrigation of HP by 2% xylocaine and intravenous infusion of atropine (100 mug per kg per hr) or metiamide (2.9 mg per kg per hr) reduced but did not abolish HP response to chemical stimulation and the pH dependency of this response. We conclude that only L- and not D-isomers of amino acids bathing the oxyntic gland area stimulate acid secretion by a local, gastrin-independent mechanism sensitive to distention pressure and pH.
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PMID:Comparison of amino acids bathing the oxyntic gland area in the stimulation of gastric secretion. 0 22

Serum gastrin concentrations were measured during fasting and after feeding in duodenal ulcer patients and in dogs before and after parietal cell vagotomy (PCV). Postoperatively, fasting serum gastrin concentrations increased significantly in man and insignificantly higher in dog. After feeding, serum gastrin reached higher values postoperatively in both man and dog. The percentage rise in food-stimulated serum gastrin after PCV was higher in dog than in man.
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PMID:Serum gastrin concentration before and after parietal cell vagotomy in man and dog. 0 57

Dogs were provided with mucosal septal pouches of the stomach and of the duodenal bulb. In some dogs a drainage gastric cannula was inserted into the most dependent portion of the stomach. In dogs which were found to secrete acid spontaneously during a control period at the start of each experiment, the bulbar puches were perfused with 0.1 M HC1 for 5-120 min. Bulbar acidification rapidly and profoundly reduced the basal acid output. In dogs which did not secrete acid spontaneously during the control periodbulbar pouches were perfused with 0.1 M HC1 for 1 h. Bulbar acidification did not significantly influence the plasma gastrin concentration and no acid was secreted from the Pavlov pouches following such acidification. The present results support the hypothesis that reduction of the intrabulbar pH may contribute to the reduction of acid secretion during interdigestive periods. The physiological significance of of mechanisms in the upper intestine which induce acid secretion following a reduction of the intraluminal pH is questioned.
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PMID:Effect of bulbar acidification on basal secretion of acid and gastrin in dog. 0 71

A method of measuring gastric secretions and emptying rates after ingestion of an ordinary (solid-liquid) meal has been developed and validated. The technique quantifies movements of volume across the pylorus using constant duodenal perfusion with a nonabsorbable marker, polyethylene glycol (PEG), which, in turn, quantifies emptying into the duodenum of another marker, [14C]PEG, incorporated in the meal. Acid and pepsin outputs can be determined without manipulation of the intragastric pH. Employing this method, we have simultaneously quantified acid, pepsin, and total secretory outputs; rates of gastric emptying of meal and secretions; and serum gastrin levels during digestion. These data characterize physiological responses to ordinary food in health.
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PMID:Measurement of gastric functions during digestion of ordinary solid meals in man. 0 10

Gastric acid output, blood-glucose, serum-gastrin and psychomotor-performance were measured in four healthy subjects one hour before and two hours after the intravenous injection of (a) 2ml saline, (b) 0.2 U/kg b.w. insulin, (c) 0.1 mg/kg b.w. bromazepam. Each subject underwent one experiment of each type. The study was layed out as a Latin-square and analysed accordingly. Gastric acid secretion was measured by means of intragastric titration and a telemetering capsule; blood-glucose and serum-gastrin levels as well as psychomotor performance as a measure of vigilance were determined in 15-minute-intervals. In the saline series (a), none of the four parameters showed any systematic variation. In series (b), a bimodal response of acid output to insulin, initial inhibition and subsequent stimulation was observed in all subjects. Serum-gastrin levels showed only a slight and transient increase in the first thirty minutes. Psychomotor performance decreased markedly with progressing hypoglycemia, and increased when glucose levels rose again. In the bromazepan series (c), acid output and psychomotor performance decreased and, after the first hour, increased almost parallely, while glucose and gastrin levels remained unchanged. In series (d), an additive effect of insulin and bromazepam occurred: acid output and psychomotor performance were lower than after insulin alone; peak acid secretion, maximal hypoglycemia and peak of serum-gastrin were shifted to the right. It is concluded that the lowered basal as well as insulin-stimulated acid secretion after bromazepam is due to the central effect of the drug, and that this effect is mediated to the gastric glands directly via autonomic nervous pathways without involving a release of endogenous gastrin.
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PMID:Gastric acid secretion, serum-gastrin levels and psychomotor function under the influence of placebo, insulin-hypoglycemia, and/or bromazepam. 0 60

Nocturnal pain and gastric hypersecretion are common in duodenal ulcer. Therefore, we investigated the antisecretory effects of a new H2-receptor antagonist, cimetidine, in 200-, 300- or 400-mg doses, taken orally at bedtime. The 200-mg dose did not cause a statistically significant change in nocturnal (midnight to 7 a.m.) acid output and had only a borderline effect on pH. However, the 300-mg and 400-mg doses significantly (P less than 0.001) lowered acid output and increased (P less than 0.01) intragastric pH. All doses caused substantial decreases in secretory volume output. After a 400-mg dose, half the patients remained anacidic for eight hours. Dose-related increases of drug blood levels were observed and correlated with the degree and duration of inhibition of acid output. Serum gastrin levels were unaffected. Cimetidine appears to be a potent inhibitor of nocturnal gastric secretion.
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PMID:Cimetidine suppression of nocturnal gastric secretion in active duodenal ulcer. 0 70

The effect of closure of a gastric cannula on the acid response to sham feeding was studied in Pavlov-pouch dogs with intact antro-duodenal regions as well as in antrectomized dogs with gastroduodenostomies. In the latter dogs, the sham feeding response was augmented by infusions of low doses of exogenous gastrin. The acid output after sham feeding in intact dogs was reduced on average by 59% by closure of the gastric cannula. In antrectomized dogs receiving a back-ground stimulation with gastrin, the response to ham feeding was not inhibited by closure of the cannula. The results suggest that the observed hypersecretory response to sham feeding after diversion of gastric acid from antrum and duodenum is mainly due to inactivation of antral inhibitory mechanisms. The pepsin secretion following sham feeding was not consistently changed by closure of the gastric cannula.
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PMID:Modification of the gastric secretory response to sham feeding by acidification of the antrum and the duodenum in dogs. 0 46

In four dogs provided with special gastroduodenal fistulas allowing for the complete separation of stomach and duodenum without interrupting the vagal connections between them, the magnitude of the gastric and intestinal phases was compared and their contribution to the total gastric response to a meal was established. A liver extract (LE) meal, confined to the stomach and maintained at pH 5.0 by an intragastric titration technique, produced acid output reaching 66% of the maximal response to histamine (MRH). Perfusion of the LE meal into the duodenum resulted in acid secretion amounting to 57% of MRH. The combination of the gastric and intestinal phases caused the highest acid output, amounting to about 90% of MRH. Gastric and intestinal phases induced separately were accompanied by a significant elevation in serum gastrin concentrations which reached the highest values when both phases were evoked simultaneously. Acidification of the intestinal meal resulted in pH-dependent inhibition of gastric secretion falling to the basal values at pH 1.0. These secretory changes were mimicked by exogenous secretin. Serum gastrin levels remained essentially unaffected by the acidification of the intestinal meal while exogenous secretin significantly lowered them. In conclusion, in the intact stomach with undisturbed nervous connections between the stomach and duodenum, a peptone meal in the intestine is capable of evoking a potent gastric acid and pepsin stimulation by a mechanism involving the release of antral hormone.
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PMID:Characteristics of intestinal phase of gastric secretion. 0 74


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