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

It has been developed by us a simple new method for producing subacute gastric ulcer in rats, combined with a novel method for the quantitative evaluation of the healing process. Fasted rats with 120-150 g were used. The animals were anaesthesized by ether and than a polyethylene chateter was orally inserted into the stomach with a fine needle inside. After the cannule reached the gastric wall, the needle was pressed gently so as to punch the gastric wall. Drugs under study were administered orally 30 min and 24 h after the puncture. Food and water were given ad libitum from 2 h after the intervention until the end (96 h) of experiments. In order to follow the healing process of subacute ulcer, the so-called tensile strength of the ulcer was determined by inflating and expressed in mmHg. The healing rate was calculated. The antiulcer drugs: Cimetidine, Famotidin, Pirenzepine and sucralfate dose dependently and significantly increased the healing rate of ulcer. Non steroidal antiinflammatory drugs: naproxen, piroxicam, indomethacin and ibuprofen significantly delayed the healing of ulcer. ASA showed tendency to delay the healing. Strong HCl (0.5 molar) significantly delayed the healing of ulcer. N-EM given subcutaneously dose dependently delayed the healing of subacute ulcer.
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PMID:Effect of cytoprotective and antiulcer drugs on the healing process of subacute gastric ulcer in rat (a new model). 259 12

The new H2-receptor antagonist mifentidine (DA 4577) was tested for its antisecretory and gastric motor effects in comparison with cimetidine and ranitidine. The Shay rat preparation (5 h) was used for studying gastric secretion; the gastric emptying of a liquid meal was chosen for studying gastric motility. All the three compounds inhibited acid secretion in a dose-dependent fashion. Calculated ED50s were 2.3, 12.2 and 92.8 mg X kg-1 for mifentidine, ranitidine and cimetidine, respectively. Therefore, in this animal model, mifentidine was about 40 times more potent than cimetidine and 5 times more potent than ranitidine. As far as gastric emptying is concerned, the effect of equiactive antisecretory doses (i.e. the respective ED50s calculated from the previously established dose-response curves) of all the three antagonists was completely different. Cimetidine delayed emptying rate, whereas ranitidine accelerated it and mifentidine was completely ineffective. However, at higher doses, also this compound affected emptying rate by reducing it dose-dependently. Gastric and duodenal ulcers were induced in the rat by dimaprit (100 mg X kg-1 intravenously) and cysteamine (250 mg X kg-1 subcutaneously), respectively. As far as gastric ulcer is concerned, the ED50s (the effective dose which protected 50% of the animals from lesions) were 0.23, 4.40 and 9.70 mg X kg-1 for mifentidine, ranitidine and cimetidine, respectively. As regards duodenal ulcer, the ED50 was 4.48 for mifentidine and 150.00 mg X kg-1 for ranitidine. In this animal model, the efficacy of cimetidine was very low. Therefore an ED50 could not be determined. In conclusion, results of the present investigation demonstrated that mifentidine is a potent antisecretory compound and an effective anti-ulcer agent in the rat.
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PMID:The effect of the new H2-receptor antagonist mifentidine on gastric secretion, gastric emptying and experimental gastric and duodenal ulcers in the rat: comparison with cimetidine and ranitidine. 286 39

The aim of this work is to establish the best treatment for patients with gastric and duodenal ulcer, by measuring the effects of antiacids and H2-receptor antagonists on gastric pH. 16 patients were studied: 9 of them had a duodenal ulcer, 2 a gastric ulcer and 5 had both. All the patients remained fasting and receiving no drug for 24 hrs. During this 24 hrs., a nasogastric tube was inserted into the stomach and the gastric content was obtained by aspiration each hour from 8 A.M. to 8 P.M. Three days after, each patient received a daily dose of 1 g of Cimetidine, and the whole procedure was repeated. The same was done with 300 mg of Ranitidine daily, 150 ml of Al-Mg antiacids daily, and at last, the same procedure was performed with the association of Ranitidine and Al-Mg antiacids at the mentioned dosage. For the statistical analysis of the data, the mean ordinate of the pH was used as a representative value of each individual's pH. Individual differences (pH with treatment minus pH without treatment) were obtained. The mean effect of each treatment was obtained averaging that differences. For comparison among different drugs, the same procedure was used. Student's paired t tests were performed in a signification level. The buffering capacity was measured in the following way: The percentage of the gastric secretion samples with pH equal or higher than 4 in each treatment and in the total number of patients was confronted with the results obtained in the same patients with no treatment. All the drugs were useful for buffering the gastric acidity, but in different intensity. The association of Ranitidine and Al-Mg antiacids showed to be the most efficient statistically when compared with Cimetidine and Al-Mg antiacids; no statistical difference appeared in the comparison with Ranitidine.
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PMID:[In vivo evaluation of the effect of antacids and H2 receptor blockaders on the intragastric pH in gastric and duodenal ulcer]. 287 55

The efficacy of a 4-week cimetidine treatment was examined by a double-blind randomized study in 37 outpatients with endoscopically verified chronic gastric ulcer. The patients received a daily dose of 3 times 1 tablet and, at night before going to bed 2 more tablet, thus a total amount of 1 g cimetidine, or cimetidine-placebo, but in case of complaints they could take in addition a mixed alkaline powder. Patients not recovering in response to a 4-week treatment, were then administered daily 5 tablets of cimetidine up to their complete recovery. Endoscopic, laboratory and clinical examinations were carried out every other week. As a result of a 4-week treatment, 56% of the cimetidine group recovered. The difference was not significant (P less than 0.2). The size of the ulcer and the intensity of the complaints were reduced significantly in both groups. The decrease in the size of the ulcer was significantly greater in the first two weeks of cimetidine treatment than in the cimetidine-placebo group (P less than 0.05). This favourable dynamics of ulcer healing was not felt in the second two weeks of treatment, and after four weeks there was no difference in the size of the residual ulcer to between the two groups. Cimetidine seemed to be a suitable drug for treating chronic gastric ulcer, since its healing rate proved to be better than that of placebo, the gain in weight also was favourable and there were no side-effects.
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PMID:Cimetidine and placebo-cimetidine in the treatment of patients with chronic gastric ulcer (a multiclinical randomized double-blind comparative study). 304 46

Prostanoids decrease gastric acid secretion and exert cytoprotective properties. The effect of several synthetic prostanoids on gastric ulcer healing was evaluated. The first trials were performed on a small number of patients with PGE2 analogs and their results were inconclusive. Two huge multicenter trials tested the efficacy of misoprostol, a synthetic PGE1 analog, in comparison to placebo and cimetidine. In the placebo-controlled trial, following 8 weeks of therapy, misoprostol 100 micrograms q.i.d was significantly better than placebo. In the cimetidine controlled trial, 2 doses of misoprostol were tested, 50 micrograms and 200 micrograms q.i.d. Ulcer healing rates following 4 weeks were 39%, 51%, and 58% in the misoprostol 50 micrograms, 200 micrograms, and cimetidine treatment groups, respectively. There was no statistically significant difference in the healing rates at 4 weeks between the misoprostol 200 micrograms and cimetidine 300 mg q.i.d groups (P = 0.16). The healing rate with the misoprostol 200 micrograms dose was significantly better than with the 50 micrograms dose (P = 0.008). Cimetidine 300 mg relieved global pain significantly better than misoprostol 200 micrograms at 2 weeks (P = 0.047) but not at 4 weeks. The 200 micrograms dose of misoprostol relieved pain significantly better than the 50 micrograms dose at 4 weeks (P = 0.019), but not at 2 weeks. All 3 treatments were well tolerated. Severe adverse events were rare. The efficacy of enprostil, another PGE2 analog, on gastric ulcer healing was also found to be better than placebo and not significantly different from ranitidine. The synthetic prostanoids, misoprostol and enprostil, appear to be safe and effective in the treatment of gastric ulcer.
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PMID:Efficacy of prostanoids in the treatment of gastric ulcer. 311

Surgically induced chronic gastric ulcers were created in rats. Cimetidine was administered for 1 year and the histological features of the gastric mucosa were studied to determine if cimetidine induced greater than normal proliferative or metaplastic changes or atypia. There were 60 rats in the study group and 51 and 55 in two control groups. The incidence of persisting chronic gastric ulcer in the cimetidine-treated study group at 1 year was 45% compared with 58% in non-treated control group (non-significant difference). There was no tendency for proliferative or metaplastic changes to be associated with cimetidine treatment--these changes reflected the presence of the chronic ulcers. Cimetidine did not induce atypia and no cases of gastric carcinoma occurred.
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PMID:The effect of cimetidine on chronic gastric ulcers in rats. 341 96

Adenylate cyclase (AC) in response to prostaglandin E2 (PGE2) and histamine was studied in morphologically different biopsy specimens from human gastric mucosa. The activities of the enzyme were log-normally distributed and did not differ between males and females. PGE2 activated AC in a concentration-dependent manner in normal gastric mucosa (n = 57), chronic superficial gastritis (GI, 18), chronic gastritis with beginning atrophy (GII, 10), chronic atrophic gastritis (GIII, 24), gastric ulcer (GU, 39), duodenal ulcer (DU, 32), and biopsies of patients operated according to Billroth II (BII, 20) and was most efficacious in GIII and BII. Histamine, which was studied in normal gastric mucosa (n = 27), DU (n = 20), GU (n = 13), and BII (n = 18), stimulated AC most efficaciously and potently in DU, was less effective in normal gastric mucosa and GU, and had no effect at all in BII. Cimetidine treatment of DU patients did not change the PGE2 action, while the degree of stimulation by histamine was reduced. The data indicate characteristic differences of the PGE2- and histamine-sensitive AC in the mucosal samples of these patients.
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PMID:Morphologically different biopsy specimens of the human gastric mucosa. II. Adenylate cyclase activity in response to prostaglandin E2 and histamine. 346 52

Curative plasmapheresis was performed in 21 patients with duodenal ulcer (DU) and in 3 patients with gastric ulcer (12 DU patients and 3 patients with gastric ulcer were taken as controls). The controls were treated by common pharmaceuticals (except Tagamet). Altogether 117 sessions of plasmapheresis were performed (an average of 5 sessions for each patient 2-3 times a week). Fibrogastroscopy was performed before and after a series of plasmapheresis (2-3 weeks after the start of therapy). In the DU patients treated by plasmapheresis ulcer cicatrization occurred in 18 days, in the controls in 27 days (p less than 0.001). In 3 patients with gastric ulcer treated by plasmapheresis cicatrization occurred on the 24th day, in the controls on the 41st day (p greater than 0.2). This method was proposed for patients with severe conditions due to the fact that a positive effect was also obtained in persons with persistently recurrent ulcers.
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PMID:[Treatment of gastroduodenal ulcer by plasmapheresis and transfusion of thawed-out autologous plasma]. 362 5

Chronic gastric ulcers were produced by injection of 20% acetic acid (0.05 ml) into the submucosal layer of the rat stomach in order to determine the effects of the prostanoid trimoprostil on the healing and recurrence of ulcers. Local injection of acetic acid solution produced large demarcated ulcers in all animals on day 5, which rapidly decreased to reach low levels on days 40-80 and then became exacerbated on day 100. The exacerbation of the ulcer is probably recurrence. Trimoprostil was administered ad libitum in drinking water containing 0.1, 0.3 and 1.0 microgram/ml (average dose 12.4, 37 and 124 micrograms/kg/day) for a period of 14 days (day 1-15) to assess its effect on healing and for a period of 40 days (day 60-100) to assess its ability to prevent recurrence. The higher two doses of trimoprostil accelerated the spontaneous healing of the ulcers. Furthermore, trimoprostil, at both doses, prevented the observed recurrence of this type of ulcer. Trimoprostil dose-dependently (30-300 micrograms/kg, p.o.) inhibited gastric secretion in pylorus-ligated rats. Cimetidine at the antisecretory dose (1 mg/ml, 132 mg/kg/day) failed to affect the healing process of gastric ulcers, but tended to prevent the recurrence of gastric ulcers. Our present study suggests that trimoprostil is a promising antiulcer drug for the treatment of chronic gastric ulcer.
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PMID:Effects of trimoprostil on healing and recurrence of acetic acid-induced gastric ulcer in rats. 380 49

Recently the Food and Drug Administration approved cimetidine for the treatment of benign gastric ulcer. Approval was based in part on the results of our large multicenter trial involving 172 patients with benign gastric ulcer between 0.5 and 2.5 cm in diameter: 87 were randomly assigned to receive cimetidine (300 mg four times daily) and 85 to receive placebo. Cimetidine treatment resulted in significantly more rapid healing than placebo; after 2 and 6 weeks of therapy, 10.0% and 44.8% of patients receiving placebo were healed, as compared to 22.6% and 65.1% receiving cimetidine. The results of our study were compared with the time-response curve previously published (0, 4, and 8 weeks of therapy). The combined data yielded linear healing rates for the first 8 weeks of therapy (r greater than 0.99 for both cimetidine and placebo). These studies can be used to define expectations for healing of benign gastric ulcer, and we recommend follow-up intervals of 8 and, if unhealed, 16 weeks.
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PMID:Healing of benign gastric ulcer: comparison of cimetidine and placebo in the United States. 388 13


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