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  • 1
    ISSN: 1432-1041
    Keywords: duodenal ulcer ; prostaglandin E2 ; gastric acid secretion ; gastrin ; trimethylprostaglandin E2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effect of varying oral doses of 11R, 16, 16-trimethyl prostaglandin E2 (TmPGE2) on meal-stimulated gastric acid secretion and serum gastrin concentrations was studied in 10 male subjects with asymptomatic duodenal ulcer disease. A liquid protein meal was infused intragastrically 0.5 h and 3.5 h after drug administration. TmPGE2 inhibited gastric acid secretion in a dose dependent manner during the first meal and no significant effect was observed during the second meal. Except for the highest dose, no TmPGE2 was detected in plasma 3 h after drug administration. The degree of inhibition of meal-stimulated gastric acid was positively correlated with the plasma level of TmPGE2, but it was not due to inhibition of postprandial gastrin release. The results indicate that oral TmPGE2 inhibits meal-stimulated gastric acid secretion but not gastrin release in humans with asymptomatic duodenal ulcer disease.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: It has been proposed that famotidine may be effective in maintaining intragastric pH ≥ 4 for up to 12 h with a single i.v. 20 mg bolus injection and thereby prevent acute stress-related mucosal haemorrhage, The present study was designed to compare a ranitidine continuous i.v. infusion (6.25 mg/h) vs. famotidine bolus injection (20 mg every 12 h) on 24-h intragastric pH and gastric acid secretion. Twenty-eight healthy volunteers (15 males, 13 females; 20–56 years) participated in two 24-h treatment periods; each test was in random order separated by 7–10 days. After an overnight fast, subjects were intubated and gastric pH and acid secretion measured hourly. Whereas ranitidine maintained gastric pH above 4 for the entire 24-h period, mean pH steadily decreased to a nadir of 2.9 and 3.7, respectively, 12 h after each famotidine injection (P 〈 0.01 vs. ranitidine). Furthermore, gastric acid secretion increased to 4.4 ± 1.2 mmol/h 12 h after famotidine injection compared to 1.1±0.3 mmol/h with ranitidine (P 〈 0.01). We conclude that ranitidine delivered as a continuous i.v. infusion (6.25 mg/h) is superior to bolus famotidine injections (20 mg) at 12-h intervals in suppressing gastric acid secretion and maintaining an intragastric pH ≥. 4. More frequent famotidine dosing, or delivery by continuous i.v. infusion, may be required to provide prolonged acid suppression.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 7 (1993), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The purpose of this study was to examine the anti-secretory effect of low doses of orally administered ranitidine on meal-stimulated gastric acid secretion and assess its pharmacokinetics. The effect of 20, 40, 60 and 80 mg of ranitidine p.o. and placebo were tested on 5 separate days (Latin square, double-blind) in 15 healthy males (mean age 35 years). Gastric acid secretion was measured prior to and for 8 h following two sequential mixed liquid meals administered at 4-h intervals. Venous blood samples were obtained at frequent intervals before and following each dose for determination of plasma ranitidine concentration by high pressure liquid chromatography. Each dose of ranitidine significantly (P 〈 0.01) decreased the peak and cumulative 4-h acid secretory responses to the first meal (range 58–93 %), and the 60 and 80 mg doses significantly inhibited the response to the second meal by 31 and 43%, respectively. Total 8-h meal-stimulated acid outputs were decreased significantly in a dose-related manner (range 38–73%). Peak plasma ranitidine occurred approximately 1 h after dosing. Ranitidine tmax, t½ and clearances were independent of dose; however, AUC and C. were dose-related. Inhibition of acid secretion was related to plasma ranitidine concentration; the mean IC50 was 27 (± 6.4) ng/ml. We conclude that modest doses (equivalent to 7–27% of the daily therapeutic dose) of ranitidine effectively suppress meal-stimulated gastric acid secretion in a dose-related manner. If these doses are of clinical efficacy, it may be possible for substantial cost savings to occur.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 31 (1986), S. 130S 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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