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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The beneficial antiulcer actions of carbenoxolone may possibly be due to an aldosterone-like component on the gastric mucosa. This suggests that aldosterone and possibly other corticoids may have antiulcer actions. The potential gastric antisecretory and antiulcer actions of aldosterone (ALDO) and desoxycorticosterone acetate (DOCA) were studied in the rat in comparison to the reference standard carbenoxolone. Stress ulcers were induced in fasted rats by the the forced exertion technique. Gastric secretion was evaluated in the five-hour pyloric ligated Shay rat model. The renal mineralocorticoid actions of these drugs were also studied in the adrenalectomized rat. Intragastric administration of carbenoxolone and DOCA, but not ALDO, significantly inhibited gastric ulcer formation in rats. Carbenoxolone given subcutaneously (s.c.) did not inhibit ulcer formation. ALDO exhibited antiulcer actions only when multiple s.c. injections were made. The antiulcer actions of DOCA and ALDO are not mediated via an inhibitory effect on gastric secretion. At all doses tested DOCA and ALDO showed significant renal effect, while carbenoxolone exhibited this effect only at the highest tested dose. These results suggest that the beneficial antiulcerogenic action of carbenoxolone is due to a direct effect on gastric mucosa and is not related to an aldosterone-like component.
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PMID:Gastric antiulcer and antisecretory effects of carbenoxolone, aldosterone and desoxycorticosterone in rats. 54 42

57 patients with a chronic gastric ulcer were treated as outpatients in a double blind comparison of carbenozolone 100 mg three times daily with the same dose of geranyl farnesyl acetate (Gefarnate). Healing rates for carbenoxolone were better than for gefarnate, but not significantly so. Nearly half the carbenoxolone-treated patients developed hypokalaemia or oedema, whereas no similar side-effects were found with gefarnate. Gefarnate, while not as effective as carbenoxolone, does appear to promote gastric ulcer healing. Its virtual absence of side-effects makes it a safe and useful drug.
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PMID:A double blind trial of carbenoxolone and geranyl farnesyl acetate in gastric ulcer. 110 73

The new non-steroidal anti-inflammatory drug (NSAID), N-(3-[3-(piperidinyl-methyl) phenoxy] propyl)-carbamoyl-methylthio]ethyl 1-(p-chlorobenzoyl) 5-methoxy-2-methyl-3-indolyl-acetate (CP 331, CAS 127966-70-5), a compound with a structure of an ester combining indomethacin (IM) and a histamine H2 antagonist, has been reported to have anti-inflammatory, analgesic and antipyretic effects. However, the influence of CP-331 on the gastroduodenal mucosa was not fully investigated. Therefore this study was undertaken to investigate the effect of CP-331 on the gastroduodenal mucosa membrane in rats. After single oral drug administration, the UD50 value (50% ulcerogenic dose) of CP-331 calculated from the incidence rate of gastric ulcer was higher than 1000 mg/kg; that for IM was 5.2 mg/kg. Moreover it was examined whether CP-331 had a preventive effect on NSAID-induced gastric damage. The results showed that the co-administration of CP-331 10-30 mg/kg prevented significantly the acute gastric mucosal injury caused by IM administration (20 mg/kg). CP-331 with anti-inflammatory activity does not cause gastric injury, moreover, because of its preventing and therapeutic effects on the damage to gastric mucous membrane induced by IM, CP-331 might be useful in the treatment of gastropathy caused by NSAID in clinic.
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PMID:Effect of a new non-steroidal anti-inflammatory combination of a histamine H2 antagonist and indomethacin on gastroduodenal mucosal membrane in rat. 136 36

It was demonstrated in experiments on rats with acetate gastric ulcer that ammonium salt tris-(2-hydroxyethyl) of iron-containing polyacrylic acid intensifies the development of granulation-fibrous tissue and promotes fuller restoration of connective-tissue polymers--collagen, noncollagenous proteins, and glycosaminoglycans in it. The biochemical results are confirmed by histological studies.
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PMID:[Analysis of the mechanism of the ulcerostatic effect of tris-[2-hydroxyethyl] ammonium salt of iron-containing polyacrylic acid]. 148 Apr 26

Adult patients with symptoms of gastric disease were randomly assigned to a treatment group (n = 103) or untreated control group (n = 89). The treatment group received 75 mg of roxatidine acetate hydrochloride at 9 PM and 12 to 13 hours later gastric juice secretion was measured with gastric x-ray films in both groups. Mean gastric juice secretion was significantly lower in the treated group (16.1 ml/12 hrs) than in the untreated controls (49.8 ml/12 hrs). Gastric juice suppression by roxatidine was 90% in patients with gastric ulcer, 74% in patients with duodenal ulcer, 63% in patients with gastritis, and 70% in patients with no evidence of disease. It is concluded that 150 mg of roxatidine daily would be adequate to treat patients with gastric diseases.
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PMID:Radiographic assessment of nocturnal gastric juice secretion after administration of roxatidine acetate hydrochloride. 167 30

The efficacy and safety of 75 mg of roxatidine acetate at night as maintenance treatment for chronic peptic ulcer disease was investigated in two double-blind randomized placebo-controlled multicenter studies. A total of 725 patients with endoscopic demonstration of a healed ulcer were recruited; 420 patients were enrolled by 28 centers in the duodenal ulcer study and 305 patients were enrolled by 24 centers in the gastric ulcer study. The duration of treatment in each study was 12 months. The primary efficacy endpoint was ulcer relapse, confirmed on scheduled endoscopy at two, four, six, nine, and 12 months or as necessitated clinically. The total ulcer recurrence rate was significantly lower in patients on active treatment: 35% and 32% of patients with a previously healed duodenal or gastric ulcer relapsed within 12 months while on roxatidine acetate, compared with 66% and 71% of patients in each study on placebo (life-table analysis, P = 0.0001). Both active and placebo treatments were well tolerated. There was no evidence of any clinically significant drug-related laboratory abnormalities, electrocardiographic changes, or changes in vital signs with either treatment. It is concluded that 75 mg of roxatidine acetate at night is a safe and effective maintenance treatment to sustain remission in patients with peptic ulcers.
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PMID:Roxatidine acetate as maintenance treatment for patients with peptic ulcer disease. The European Cooperative Roxatidine Study Group. 167 31

Roxatidine acetate is a histamine H2-receptor antagonist which, after almost complete oral absorption (greater than 95%), is rapidly converted to its active metabolite, roxatidine, by esterases in the small intestine, plasma and liver. Roxatidine is a potent inhibitor of basal and stimulated gastric acid secretion in animals and humans and, like most other H2-receptor antagonists, has no anti-androgenic effects and does not interfere with the hepatic metabolism of other drugs. Large-scale trials have shown that roxatidine acetate 150mg per day is as effective as standard doses of cimetidine and ranitidine in the treatment of patients with duodenal or gastric ulcer, and that roxatidine acetate 75mg in the evening is likely to become a 'standard' regimen for the prevention of peptic ulcer recurrence. Preliminary data also suggest that roxatidine acetate may be useful in the treatment of reflux oesophagitis and stomal ulcer, and in the prevention of pulmonary acid aspiration. Roxatidine acetate is an H2-receptor antagonist which has been well tolerated in clinical trials. However, broader experience is required before definitive statements about tolerability relative to other H2-receptor antagonists can be made, and before the role of roxatidine acetate in the treatment of reflux oesophagitis and stomal ulcer, and the prophylaxis of acid aspiration pneumonitis, can be clearly defined.
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PMID:Roxatidine acetate. A review of its pharmacodynamic and pharmacokinetic properties, and its therapeutic potential in peptic ulcer disease and related disorders. 171 23

Rat gastric mucosal blood flow, hydrochloric acid (HC1) secretion, and morphological changes of parietal cells were studied by light and electron microscopy using histochemical techniques. Mucosal blood flow of restrained rats was remarkably decreased compared with that of control rats, whereas the acetylcholinesterase activity, demonstrated by the method of Karnovsky and Roots, was significantly increased especially near the ulcer. In contrast, the differences in volume, acidity and acid output of gastric juice were not significant between control and restrained rats. Hypersecretion of HC1 induced by a parasympathetic stimulant, bethanechol, was inhibited by blood loss or infusion of cytochalasin B, an actin depolymerizing agent. 14C-aminopyrine accumulation in the primary cultured parietal cells was decreased by the treatment with hypoxia and cytochalasin B. These treatments also prevented the increase of 14C-aminopyrine accumulation induced by bethanechol. Actin filaments were evident in the cytoplasm of the parietal cells, particularly around the intracellular canaliculi and beneath the plasma membrane using the FITC-labeled phalloidin reaction and transmission electron microscopic observations of uranyl acetate block stained preparations following heavy meromyosin decorations. Ultrastructural studies of the parietal cells in restrained rats revealed that intracellular canaliculi were dilated with loss of microvilli. Actin filaments were noted to be disassembled, and granular with focal aggregation of actin filaments. Hypoxic vacuoles were also found in the cytoplasm. Treatments with blood loss and cytochalasin B infusion in the in vivo model, and hypoxia and cytochalasin B in the in vitro model, resulted in the similar changes. These observations indicate that actin filaments in the parietal cells of restrained rats may be depolymerized by ischemia. As the result, HC1 secretion would not be enhanced even if the parasympathetic nerves are excessively stimulated in the gastric mucosa. Thus, disturbances of the gastric mucosal microcirculation are considered to be important in the pathogenesis of the stress-induced gastric ulcer.
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PMID:[Studies on the mechanism of restraint-induced gastric ulcer--with special reference to mucosal ischemia and gastric secretion]. 232 29

Stimulating effect of I-ethoxy silatrane on healing of acetate derived stomach ulcer was studied in rats. The drug was shown to inhibit lipid peroxidation and free-radical oxidation in blood and gastric tissues as well as to accelerate reparation in ulcerous zone. I-Ethoxy silatrane interacted with artificial membranes and affected the respiration rate in liver mitochondria. Membranetropic effect of I-ethoxy silatrane appears to be involved in the drug ulcerostatic effect.
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PMID:[1-Ethoxysilatrane: ulcerostatic effect and its possible mechanisms]. 236 53

The effects of a new H2-receptor antagonist, roxatidine acetate, have been investigated in both clinical and pharmacodynamic trials in Europe and the United States. A series of four double-blind randomized studies are reviewed, reporting the effects of different dose regimens of roxatidine acetate compared with ranitidine and placebo in healthy volunteers using continuous intragastric pH monitoring. These pharmacodynamic studies clearly demonstrate that roxatidine acetate is an effective gastric antisecretory agent, which is up to twice as potent as ranitidine. The results of several clinical studies of roxatidine acetate in patients with gastric as well as duodenal ulcer conducted in Europe, Japan, and the United States are also reviewed. These studies show that roxatidine acetate is comparable to other potent H2-receptor antagonists in terms of cumulative healing rates, pain relief, and safety. Overall, the pharmacodynamic and clinical data indicate that the efficacy of roxatidine acetate 75 mg twice-daily (b.i.d.) does not differ significantly from ranitidine 150 mg b.i.d. Roxatidine acetate is equally effective in the treatment of peptic disease including gastric ulcer, duodenal ulcer, and reflux esophagitis.
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PMID:Safety and efficacy of roxatidine acetate. Evidence from pharmacodynamic and clinical trials. 257 21


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