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  • 1
    Electronic Resource
    Electronic Resource
    Effect of cimetidine on pentagastrin- and meal-stimulated gastric acid secretion and serum gastrin before and after one month of daily cimetidine treatment (1978)
    Springer
    Inflammation research 8 (1978), S. 406-406 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusions Compared to the pretreatment studies, after 1 month of daily C: (1) 300 mg of oral C produced significantly less inhibition of peptone-stimulated gastric acid secretion (Table 1); (2) serum gastrin response to PM was significantly greater; and (3) the duration of the inhibitory effect of 300 mg of C i.v. on PG-stimulated gastric acid secretion was significantly shortened (Table 1).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01968653
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of 11R, 16, 16-trimethyl prostaglandin E2 on meal-stimulated gastric acid secretion in duodenal ulcer subjects (1986)
    Springer
    European journal of clinical pharmacology 31 (1986), S. 281-284 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00981124
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of enprostil on the gastroduodenal mucosa of healthy volunteers (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 4 (1990), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Enprostil is a synthetic dehydro-prostaglandin E2 with gastroduodenal ulcer-healing and mucosal-protective properties. One hundred and three healthy volunteers were randomized to receive capsules of enprostil 35 μg b.d. (the clinically recommended dose), enprostil 70 μg b.d., or placebo b.d. All underwent endoscopic assessment of the gastroduodenal mucosa, scored using a 0–4 scale, at baseline and on Days 3, 7, 14, 21 and 28 of dosing. Mean and median maximum scores demonstrated a dose response, and the mean maximum scores were statistically significantly higher for both enprostil groups on each endoscopy day when compared with placebo. The majority of enprostil-treated subjects had petechial haemorrhages. The proportion of volunteers with small white-based mucosal breaks (erosions) was significantly higher for the fundus in the enprostil 70-μg group on Days 21 and 28 when compared with placebo, but there were no significant differences between treatment groups for any area on the other study days. The 70-μg dose was
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.1990.tb00508.x
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  • 4
    Electronic Resource
    Electronic Resource
    The impact of H2-receptor antagonists on the complications, morbidity and mortality of peptic ulcer disease (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 1 (1987), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The epidemiology and character of peptic ulcer has changed over the last 20 years, with only some of the change being due to the introduction of H2-receptor antagonists in the mid-1970s. There is evidence that duodenal ulcer was declining before this change in therapeutics. H2-receptor antagonists have, however, greatly reduced the morbidity and the time off work due to peptic ulcer disease. There is no strong evidence, however, that mortality due to peptic ulcer disease, which was already relatively small, has been reduced. The incidence of complications such as gastric haemorrhage, perforation and obstruction, may have increased in elderly patients. This may be associated with independent variables, such as increased use of non-steroidal anti-inflammatory drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.1987.tb00655.x
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  • 5
    Electronic Resource
    Electronic Resource
    Review article: gastroduodenal bicarbonate secretion (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 8 (1994), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The gastroduodenal epithelium is covered by an adherent mucus layer into which bicarbonate is secreted by surface epithelial cells. This mucus-bicarbonate barrier is an important first line of defence against damage by gastric acid and pepsin, and has been demonstrated in all species including human. Similar to gastric acid secretion, regulation of gastric and duodenal bicarbonate secretion can be divided into three phases: cephalic, gastric and duodenal. In humans, sham-feeding increases bicarbonate secretion in both the stomach and duodenum which is mediated by cholinergic vagal fibres in the stomach, but seems to be noncholinergic in the duodenum. Gastric distention and luminal acidification increases gastric bicarbonate production. Whereas there are no data relating to the gastric phase of human duodenal bicarbonate secretion, in animals, food and acid in the stomach independently stimulate duodenal bicarbonate output. To date, the duodenal phase of human gastric bicarbonate secretion has not been studied, but data from animals reveal that duodenal acidification augments bicarbonate secretion in the stomach. In all species tested, direct acidification of the duodenum is a potent stimulant of local bicarbonate production. In humans, the pH threshold for bicarbonate secretion is pH 3.0. Mediation of gastroduodenal bicarbonate secretion is provided by a variety of agonists and antagonists, tested mainly in animals, but some have been evaluated in humans. Prostaglandins of the E class and VIP are major factors that control bicarbonate secretion. Bicarbonate secretion, and the mucus-bicarbonate layer in general, is adversely effected by ulcerogenic factors such as aspirin, NSAIDs, bile salts, and cigarette smoking. Furthermore, duodenal ulcer patients have an impairment in bicarbonate production within the duodenal bulb, at rest and in response to stimulation. These findings indicate that the mucus-bicarbonate barrier is an important first line of defence in the pathogenesis of peptic ulcer disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.1994.tb00319.x
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  • 6
    Electronic Resource
    Electronic Resource
    Cimetidine decreases aspirin-induced gastric mucosal damage in humans (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 1 (1987), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aspirin induces gastric mucosal damage in animals and humans. The purpose of this study was to examine whether cimetidine protects the human gastric mucosa from acute aspirin-induced damage. Eight healthy subjects were studied on 4 separate days. Cimetidine, 400 mg, or placebo was given orally 1 hour before initial endoscopy. The stomach was isolated and atropine given to suppress basal acid secretion. Each study consisted of four 15 min periods during which an acidic test solution was instilled into the stomach. During the second period only, either aspirin (1300 mg, 36 mmol) or control for aspirin (36 mmol HCl) was added to the test solution. Ion fluxes and gastric mucosal potential difference were measured, and endoscopy performed following each test. After placebo, aspirin significantly altered hydrogen ion flux and potential difference versus basal and control. Cimetidine decreased the damaging effect of aspirin. Endoscopic scores increased after aspirin plus placebo, whereas they remained unchanged after aspirin plus cimetidine. Therefore, cimetidine decreased aspirin-induced gastric mucosal damage in humans. As gastric acidity was identical during all studies, the effect of cimetidine was independent of gastric acid secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.1987.tb00638.x
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  • 7
    Electronic Resource
    Electronic Resource
    Gastric acid suppression is greater during intravenous ranitidine infusion versus bolus injections of famotidine (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 7 (1993), S. 0 
    Details
    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
    URL: http://dx.doi.org/10.1111/j.1365-2036.1993.tb00130.x
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  • 8
    Electronic Resource
    Electronic Resource
    Anti-secretory effects and pharmacokinetics of low dose ranitidine (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 7 (1993), S. 0 
    Details
    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
    URL: http://dx.doi.org/10.1111/j.1365-2036.1993.tb00115.x
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  • 9
    Electronic Resource
    Electronic Resource
    Duodenal bicarbonate secretion in humans (1986)
    Springer
    Digestive diseases and sciences 31 (1986), S. 130S 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01309337
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