Ranitidine plus Bromazepam in the Treatment of Duodenal Ulcer: Effect on Gastric Acid Secretion

1989 ◽  
Vol 17 (1) ◽  
pp. 55-61 ◽  
Author(s):  
E. García-Oyola ◽  
W. I. Curioso

The effect of adding bromazepam to treatment of duodenal ulcer with ranitidine was investigated in 30 out-patients. Under double-blind conditions one group of 15 patients received, for 14 days, 300 mg ranitidine and 6 mg bromazepam in the evening as a single dose. The other group received the same dose of ranitidine together with placebo, also for 14 days. In addition to measurements of gastric acid secretion after fasting and following histamine provocation, psychological ratings (Hamilton Anxiety Rating Scale and Zung Self-Assessment Scale for Anxiety) were carried out. Basal acid secretion was the same in both groups. During treatment, maximal acid output was significantly lower in the group of patients taking bromazepam than in those taking placebo. Similarly, significant differences were seen in favour of bromazepam in the psychological tests. It is concluded that these results confirm that bromazepam exerts a significant influence on acidity, over and above the effect of ranitidine. This effect, in all probability, is modulated by the emotional environment of individuals.

1995 ◽  
Vol 269 (5) ◽  
pp. G721-G728
Author(s):  
R. K. Rao ◽  
S. Pepperl ◽  
F. Porreca

Stimulation of gastric acid secretion by secretagogues was measured in developing rats by in vivo and in vitro techniques. Basal acid outputs in vivo were very low in 8- and 14-day-old rats compared with those in 20- and 30-day-old rats. In 20-day-old rats, all secretagogues increased acid output in vivo, whereas only carbachol, pentagastrin, and sulfated cholecystokinin octapeptide (CCK-8S) were active in 14-day-old rats. In contrast, basal acid output in vitro and stimulation by secretagogues did not differ significantly with age. CCK-8S-stimulated acid output in vitro in 14-day-old rats was blocked by L-365,260, L-364,718, tetrodotoxin, and atropine, but not by hexamethonium, whereas gastrin-stimulated acid output was blocked only by L-365,260. Furthermore, acid output in vivo was elevated three- to fourfold by subcutaneous naloxone-methiodide or L-364,718, but not by L-365,260, in 14-day-old rats; none of these antagonists produced an effect in 20-day-old rats. These studies show that low basal gastric acid output in neonatal rats is caused by tonic inhibitory regulation by endogenous regulatory peptides.


2000 ◽  
Vol 7 (2) ◽  
pp. 57-62 ◽  
Author(s):  
Marc A. Ilies ◽  
Claudiu T. Supuran ◽  
Andrea Scozzafava

Zinc, magnesium, aluminum and copper complexes of several potent, clinically used carbonic anhydrase (CA) sulfonamide inhibitors, such as acetazolamide, methazolamide, ethoxzolamide and benzolamide were tested for their possible applications as antacids, in experimental animals. Gastric acid secretion parameters 3 days after treatment with these CA inhibitors (2 × 500 mg, twice a day), in dogs with chronic gastric fistulas, led to the observation that the gastric acid parameters BAO (the basal acid output), and MAO (the maximal acid output after stimulation with histamine) were drastically reduced, as compared to the same parameters in animals that did not receive these enzyme inhibitors. These are promising results for the possible use of metal complexes of heterocyclic sulfonamides as treatment alternatives (alone or in combination with other drugs) for gastric acid secretion imbalances.


1977 ◽  
Vol 13 (1) ◽  
pp. 115-124 ◽  
Author(s):  
Frederick W.K. Chen ◽  
Ho Soon Teck ◽  
Sultan M.M. Karim

1982 ◽  
Vol 243 (2) ◽  
pp. G127-G133
Author(s):  
L. M. McLeay ◽  
J. M. Fitzgerald

Effects on ovine gastric function of procedures that increase intestinal unsaturated fatty acid content are unknown, and the present aim was to compare the effects of duodenal unsaturated and saturated fatty acids on gastric secretion in conscious sheep. During the maximal gastric secretory response to a meal, 10 ml gallbladder bile alone or with myristic, palmitic, and stearic acids and oleic, linoleic, and linolenic acids were infused into the duodenum at a rate of 5 g fatty acid . h-1 for 1 h. Compared with control 154 mM NaCl (100%), acid output was reduced to 4-7% of control with infusion of oleic, linoleic, and linolenic acids and myristic acids plus bile. Reductions in acid secretion persisted for up to 5 h from the end of infusion. In contrast, the infusion of palmitic and stearic acids with bile caused mean maximal reductions in acid output, respectively, to only 64 and 55% of control, and levels returned to control within 1 h of the end of infusion. Bile infusion alone caused no reduction in acid secretion. Under the conditions used, C18 unsaturated fatty acids and myristic acid were potent inhibitors of ovine gastric acid secretion. The lesser effects of palmitic and stearic acids were probably related to their reduced solubility and absorption.


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