Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four hour intragastric acidity was measured in nine volunteer subjects in a single-blind placebo-controlled cross-over study comparing the effects of famotidine with ranitidine. The volunteer subjects received famotidine (40 mg at night), famotidine (20 mg at night), ranitidine (300 mg at night) or placebo in a predetermined random order. Twenty-four hour intragastric acidity was measured after the seventh dose of each drug or placebo. Famotidine (20 mg), famotidine (40 mg) and ranitidine, all caused a significant decrease of intragastric nocturnal acidity when compared with placebo (P less than 0.01), with no effect during the daytime (P greater than 0.05). Treatment with all the drugs caused a significant rise of fasting plasma gastrin concentration compared with placebo (P less than 0.05).
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PMID:Effect of oral famotidine on 24-hour intragastric acidity. 289 Jan 50

The effect of histamine H2-antagonists on serum gastrin concentration and histamine-stimulated gastric acid secretion was studied in gastric lumen-perfused rats in which changes in the intragastric pH were limited by using 2.5 mM propionate-succinate buffer as perfusate. The gastric acid secretion was measured by the titration of the acidity of gastric juice with 0.05 N NaOH. The serum gastrin levels were determined in the blood that was obtained simultaneously with gastric juice by radioimmunoassay. The gastric acid secretion was inhibited by these histamine H2-antagonists--cimetidine, famotidine, ranitidine and TZU-0460 administered intravenously. Within the dose-response range of the inhibition of gastric acid secretion, cimetidine and ranitidine increased significantly the serum gastrin levels, but famotidine and TZU-0460 did not. The doses of famotidine and TZU-0460 which were used to increase the serum gastrin levels were found to be higher than those for the maximal inhibition of gastric acid secretion. They also presented a dose-response curve to the serum gastrin levels similar to cimetidine and ranitidine. The findings suggest that histamine H2-antagonists have a potency to increase serum gastrin levels to that of the inhibition of gastric acid secretion.
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PMID:[Effect of histamine H2-antagonists on serum gastrin levels in gastric lumen-perfused rats]. 290 May 46

Nine healthy volunteers were studied on the seventh day of dosing at 21:00 h with nizatidine 150 mg (N 150), nizatidine 300 mg (N 300), ranitidine 300 mg (R 300), or placebo, given in a predetermined random order. The double-blind 24 hour studies, using the Royal Free Hospital standard protocol, simultaneously measured intragastric acidity and plasma gastrin concentration. Compared with placebo, subjects responded to dosing with each H2-antagonist by a significant decrease of 24 hour intragastric acidity (N 150-45%; N 300-49% R 300-56%; p less than 0.01) and a significant rise of plasma gastrin concentration (N 150 + 20%; N 300 + 27%; R 300 + 58%; p less than 0.01). All three drug regimens caused similar significant decreases of nocturnal acidity (N 150-72%; N 300-79%; R 300-85%; p less than 0.01) and increases of nocturnal plasma gastrin concentration (N 150 + 41%; N300 + 52%; R 300 + 80%; p less than 0.01). Dosing with ranitidine 300 mg at 21:00 h also caused a simultaneous significant decrease of morning acidity (-32%; p less than 0.05) with a significant increase of plasma gastrin concentration (+36%; p less than 0.05), but the antisecretory effects of nizatidine 150 or 300 mg at 21:00 h were only observed during the night, with no effect during the morning. No drug regimen had any effect on acidity or plasma gastrin in the afternoon or early evening.
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PMID:Twenty four hour intragastric acidity and plasma gastrin concentration in healthy volunteers taking nizatidine 150 mg, nizatidine 300 mg, ranitidine 300 mg, or placebo at 21:00 h. 290 94

The roles of plasma gastrin and duodenal acidity in duodenal ulcer disease remain unclear. In this pathophysiologic study, plasma gastrin and dual gastro-duodenal pH were measured before, during, and after cephalic stimulation (modified sham feeding) and the ingestion of a meal in 16 duodenal ulcer (DU) patients and twelve healthy subjects. Gastrin levels were significantly higher in DU patients both in the fasting state (42.5 ng/l vs. 22.5 ng/l, p less than 0.001) and after the meal (130 vs. 60, p less than 0.02). Two separate patient subsets were identified: a "hypergastrinemic" (HRG) group exhibiting exaggerated gastrin responses and a "Normogastrinemic" (NOG) group comprised of patients with gastrin levels similar to those of controls. Only the HRG group exhibited a significant gastrin response to sham feeding. Both patient groups exhibited a delayed onset of duodenal acidity and delayed peak acid response after feeding indicative of delayed gastric emptying of the acid load. The HRG group exhibited a longer duodenal acid exposure and a prolonged return to premeal pH levels, suggesting a defective switch-off mechanism of acid secretion after duodenal acidification.
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PMID:Effects of sham feeding and a meal on plasma gastrin and duodenal pH in normal and duodenal ulcer patients. 293 Feb 86

Twenty-four-hour intragastric acidity and plasma gastrin concentration were measured in healthy subjects (n = 16), and patients with duodenal (n = 12) or gastric (n = 10) ulceration, or pernicious anaemia (n = 8). Median integrated 24-hour intragastric acidity was highest in duodenal ulcer patients and lowest in pernicious anaemia patients (1148 and 0 mmol.hour litre-1, respectively). Median integrated 24-hour plasma gastrin was highest in pernicious anaemia and lowest in the healthy subjects (9886 and 238 pmol.hour litre-1, respectively). Pernicious anaemia patients have unremitting hypergastrinaemia throughout the 24 hours. The results of this study not only provide a reference range of acidity and plasma gastrin in health and disease, but also will act as a baseline for future studies using antisecretory drugs.
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PMID:Twenty-four-hour intragastric acidity and plasma gastrin concentration in healthy subjects and patients with duodenal or gastric ulcer, or pernicious anaemia. 297 25

Simultaneous 24-hour intragastric acidity and plasma gastrin concentrations were measured in 12 duodenal ulcer patients before and on the twenty-eighth day of treatment with either ranitidine 150 mg b.d. or omeprazole 20 mg o.m. Median integrated 24-hour intragastric acidity was decreased significantly from 1148 to 490 and 36 mmol.hour litre-1 during treatment with ranitidine and omeprazole, respectively, whilst median intragastric 24-hour plasma gastrin was raised significantly from 328 to 799 and 1519 pmol.hour litre-1 respectively. When the results of all 48 experiments were considered together, there was a significant inverse correlation between the 24-hour integrated values for intragastric acidity and plasma gastrin concentration. Both drugs caused a significant elevation of plasma gastrin throughout the 24 hours, although ranitidine had no effect on intragastric acidity from 1900 to 2200 hours. When compared with similar profiles of acidity and gastrin in pernicious-anaemia patients, the modest elevations of plasma gastrin observed in this study suggest that neither drug will be associated with clinically relevant enterochromaffin-like cell proliferation in duodenal ulcer patients.
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PMID:Twenty-four-hour intragastric acidity and plasma gastrin concentration before and during treatment with either ranitidine or omeprazole. 297 26

Exposure of the stomach to tumoricidal doses of radiation is associated with functional and morphological changes. The experimental data have been mainly obtained from studies of whole body irradiation of the stomach. We investigated the separate effect of irradiation on the surgically exposed stomach with doses of between 3 and 30 Gy. A dose-dependent decrease in free and total acidity was observed with relatively low doses (5-9 Gy). Serum pepsinogen and serum gastrin levels increased following irradiation with doses ranging from 5 to 15 Gy. Two phases of increased regenerative activity were documented (between the 1st and 3rd weeks and between the 4th and 8th weeks). No radioprotective effect was observed when sucralfate or misoprostol were utilized. Further investigations are mandatory in order to find an effective radioprotector for the irradiated stomach.
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PMID:Functional and morphological alterations following isolated rat stomach irradiation. A model for estimation of radiation injury. 297 4

Changes on levels gastric acidity, on serum gastrin, cAMP and cGMP levels were studied in 18 healthy volunteers after either stimulation (injection of 0.2 IU of soluble insulin/kg body weight to a group of 9 subjects) or stimulation and inhibition (injection of insulin plus atropine per os to the other group of 9 subjects) of the vagus nerve. After vagus nerve stimulation, gastric acid levels, serum gastrin and cGMP were raised and cAMP reduced. After stimulation and inhibition of vagus nerve, gastrin and cAMP were increased, cGMP reduced and gastric acid levels remained unchanged. These findings suggest that the vagus nerve, and more particularly the acetylcholine released from its metaganglionic fibers, stimulate parietal cells provoking acid secretion, and also stimulate G cells with subsequent gastrin secretion through cGMP.
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PMID:[Secretion of gastric acid, gastrin and cyclic nucleotides in relation to the action of the vagus nerve]. 298 23

This paper reviews the relationship between gastric acid secretion and infection and the protective role of gastric acid as a primary bactericidal barrier and modulator of gastrin section. Gastric acid is bactericidal at pH 3 or less, but reduction of acidity predisposes to infection with a wide variety of bacteria. Bacterial infections or hyperpyrexia may be associated with a marked reduction in gastric acid secretion, and Campylobacter pylori has been suggested as one cause of epidemic hypochlorhydria. Achlorhydria is also associated with hypergastrinaemia with levels 20-fold higher in pernicious anaemia patients than normal subjects. Treatment with antisecretory drugs is associated with hypergastrinaemia with gastrin levels 2- to 5-fold higher than with placebo, and the gastrin levels correlate with the degree of acid suppression. The possible relationship among infection, acid suppression, hypergastrinaemia, and the development of enterochromaffin cell hyperplasia and possible carcinogenesis is reviewed.
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PMID:The protective role of gastric acid. 306 34

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of omeprazole are reviewed. Omeprazole, a substituted benzimidazole, has a unique site and mechanism of action because it inhibits the proton pump--i.e., hydrogen, potassium adenosine triphosphatase (H+,K+-ATPase)--and consequently blocks the final common step in the gastric acid secretory pathway. Omeprazole inhibits basal and histamine-, gastrin- and pentagastrin-stimulated gastric hydrochloric acid secretion. It produces a dose-dependent reduction in gastric acidity, gastric acid output, and gastric juice volume and has variable effects on pepsin secretion. Omeprazole has no documented effect on esophageal motility or lower esophageal sphincter pressure. Omeprazole is variably absorbed from the gastrointestinal tract, and food appears to decrease the rate, but not the extent, of drug absorption. The drug is approximately 95% bound to plasma proteins and is metabolized to inactive components that are enterohepatically or renally eliminated. Omeprazole is more effective (in most studies) than H2-receptor antagonists in treating duodenal ulcer, at least as effective in treating benign gastric ulcer, and more effective in treating reflux esophagitis. Omeprazole has been used successfully in patients with Zollinger-Ellison syndrome refractory to treatment with H2-receptor antagonists. Gastrointestinal complaints (nausea and diarrhea) are the most commonly reported adverse effects associated with omeprazole therapy. The most frequently reported laboratory abnormality occurring with omeprazole use is elevation of serum aspartate aminotransferase and alanine aminotransferase concentrations. Omeprazole will serve a valuable role in the management of gastrointestinal tract ulcers and hypersecretory conditions.
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PMID:Therapeutic evaluation of omeprazole. 306 85


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