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At least 1,333 records · Page 74Linked to original sources
PubMed1984

Influence of 'cytoprotective' drugs (carbenoxolone, zolimidine, prostanoic acid) on mucus secretion in patients with gastric ulcer.

We have studied gastric mucus secretion after carbenoxolone, zolimidine and prostanoic acid short term treatment (28 days) in patients with endoscopically demonstrated peptic gastric ulcer of the lesser curvature. Six patients were treated with carbenoxolone (300 mg/day), 6 with zolimidine (1200 mg/day) and 6 with prostanoic acid (2 g/day). All of them were submitted to gastric juice collection, before and after treatment, during 1 h at fast. On the samples of gastric juice, taken at 15 min intervals, the protein component (PC), glucosamine (GL), fucose (FU), the free N-acetyl-neuraminic acid (NANA) and sulphate groups (SG), were determined by biochemical methods. We have observed a significant increase of PC after zolimidine (P less than 0.02) and prostanoic acid (P less than 0.05) treatment, without significant variations of the other mucus components. No significant variations of mucus secretion after carbenoxolone treatment. If we compare the three drugs, we can see a significant increase of PC after zolimidine (P less than 0.005) and after prostanoic acid (P less than 0.001), compared with the results obtained after carbenoxolone. There are no significant variations of basal and stimulated (pentagastrin 6 mcg/Kg i.v.) secretory volume and acid output before and after treatment in the three groups of patients.

Adult↗
PubMed1984

Interrelationships between the chemical structure of prostanoids and prostacyclins and their cytoprotective effects on the ethanol-induced gastric mucosal damage in rats (a comparative experimental study).

Structurally modified prostaglandins have been synthesized, PGF2 alpha skeleton being substituted at the 13 and 17 position. The prostacyclin analogues were modified at the 3,13 or 17 positions of the prostacyclin skeleton. The effect of these compounds was studied on the development of gastric mucosal damage produced by the intragastric administration of 96% ethanol. The different compounds were given intraperitoneally 30 min before the administration of ethanol. The number and severity of gastric mucosal lesions (ulcers) were recorded without and with the use of different compounds. The prostanoids and prostacyclin analogues were given in doses of 1, 5, 25 or 126 micrograms/kg. Among the tested compounds several fairly active molecules could be found. The significance and practical usefulness of these modifications of prostaglandins and prostacyclins are discussed with special respect to the stereochemistry of molecules.

Animals↗
PubMed1984

Evidence for thimerosal induced cytoprotection on rat stomach.

Intragastrically administered thimerosal protects against ethanol induced ulceration with an ID50 of 1.6 mg/kg body weight. In contrast, intravenously administered thimerosal exhibits an ID50 of greater than 30 mg/kg. The antiulcerogenic effect of thimerosal persists for at least 20 hours before allowing gastric ulcers to be induced by ethanol. Intragastric application of thimerosal protects against acetyl salicylic acid induced with an ID50 of 6.8 mg/kg. Stress ulceration is inhibited by thimerosal with an ID50 of 9.2 mg/kg body weight. Investigations on the structure-activity relationship show that it is the mercury moiety and not the thiosalicylic acid moiety which is responsible for the inhibition by thimerosal.

Animals↗
PubMed1984

Gastric cytoprotection by pirenzepine: role of endogenous catecholamines.

Acute gastric ulcerations were produced in fasted rats by pylorus ligation or by administration of polymyxin B or absolute ethanol. In pylorus-ligated rats pirenzepine 25 mg/kg per os decreased by about 50% the ulceration score, without affecting gastric acid and pepsin output. A similar percentage inhibition of ulceration score with no change of gastric acidity was obtained with pirenzepine 5 mg/kg per os in the case of gastric lesions provoked by polymyxin B. Ethanol-induced gastric lesions were also markedly reduced by pirenzepine, with 50% inhibition occurring with the dose of 25 mg/kg. The release of catecholamines from rat isolated gastric tissue during stimulation of sympathetic periarterial nerves was significantly reduced by pirenzepine 1 X 10(-6) g/ml. The present results indicate that pirenzepine significantly reduced gastric lesions induced by various stimulants; the protective effect of pirenzepine did not appear to be related to increased sympathetic tone.

Animals↗
PubMed1984

Functional cytoprotection by certain antacids.

The effect of different antacids has been investigated on ulcer development, parameters of mucus barrier disruption and gastric PGE2 content in rats. Al(OH)3-containing antacids inhibit gastric ulcer formation induced by alcohol or acetylsalicylic acid (ASA). Changes in parameters of mucus barrier disruption evoked by sodium taurocholate can be significantly diminished by treatment with antacids. This protective effect of antacids is abolished in animals pretreated with indomethacin. PGE2 contents both in gastric mucosa and instillate are increased by pretreatment with antacids. PGE2 content in gastric mucosa or instillate diminished by sodium taurocholate can be normalized by antacid treatment. Although acidic isotonic or acidic hypertonic solutions increase gastric PGE2 content, they are not ulceroprotective. In these solutions, detectable amounts of released PGE2 are minimal. Under in vitro circumstances, the lifetime of PGE2 in gastric juice is shortened by decreasing pH. It has been concluded that Al(OH)3-containing antacids increase PGE2 content in the gastric mucosa. Furthermore, they are capable of lengthening the lifetime of PGE2 in the gastric content. Thus, the clinical use of Al(OH)3-containing antacids in low doses is to be emphasized in the management of gastric ulcer disease.

Animals↗
PubMed1983

Cytoprotective effect of vitamin A and its clinical importance in the treatment of patients with chronic gastric ulcer.

The effects of vitamin A were studied on the basal and maximal gastric secretory responses of 12 patients; and on healing in 60 patients with chronic gastric ulcer. The effect of vitamin A on ulcer healing was evaluated by a multiclinical, multicentre, randomized, prospective study in which the patients were divided into three groups. In group A the patients were treated with antacids only; in group B the patients were given antacids plus vitamin A (in doses of 3 X 50.000 U orally); and in group C the patients received antacids, vitamin A plus cyproheptadine (in doses of 3 X 4 mg orally). The treatment lasted four weeks. At the beginning and the end of treatment endoscopies were performed and ulcer sizes were measured planimetrically. Various other parameters such as ulcer index, antacid consumption and laboratory parameters were also evaluated during the four-week treatment. It was observed that: (i) vitamin A (given in doses of 100.000 U i.m.) decreased neither basal nor maximal gastric secretory responses; (ii) the number of patients with completely healed gastric ulcer was significantly higher (P less than 0.05) in groups B and C than in group A; (iii) the extent of ulcer reduction was significantly higher (P less than 0.01) in groups B and C than in group A; (iv) no significant changes were observed in ulcer index and antacid consumption during the four-week treatment in the different groups of patients; (v) the reduction of ulcer size was significantly greater (P less than 0.01) in the group treated with antacids plus vitamin A than in the group treated with antacids only, at two weeks of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Antacids↗
PubMed1983

FCE 20700, a cytoprotective PGE2 derivative, does not interfere with the antiinflammatory activity of indomethacin.

A study was made of the interaction between FCE 20700 (11-deoxy-13,14-didehydro-16(S)-methyl-PGE2 methylester) at a fixed dose of 250 mcg/kg and the ulcerogenic and antiinflammatory effect of indomethacin (I) on rat carrageenin paw edema. The combination tested showed the same antiinflammatory effect as I alone: potency ratio FCE 20700 + I/I was 1.03, demonstrating the lack of interaction between the two compounds. Moreover the gastric lesions in FCE 20700 + I treated rats were markedly reduced, allowing the dosage of I to be increased by about three times without increasing its ulcerogenic effect.

Animals↗