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

In the present paper, effects of scopolia drugs (scopolamine, anisodine, anisodamine) on experimental gastric mucosal lesion models in rats were investigated. Scopolia drugs were found to be effective anti-ulcer agents in three experimental gastric ulcer models (i.e. cold-restraint stress induced ulcer, indomethacin induced ulcer and acetic acid induced chronic ulcer) in rats in a dose dependent manner. Biochemical analysis of gastric juice and blood showed that scopolia drugs could inhibit gastric acid secretion and pepsin activity, increase gastric barrier mucus and concentration of serum gastrin, suggesting that these actions may contribute to its anti-ulcer effect.
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PMID:[Effect of scopolia drugs on the gastric mucosal lesion in rats]. 223 28

Anti-ulcer activities of fruits of Trichosanthes kirilowii Maximowicz var. japonica Kitamura (50% ethanolic extract, TKE) were investigated in rats. TKE, at doses of 100-1000 mg/kg, showed potent protection against experimental gastric lesions, namely, those induced by water-immersion, histamine, serotonin, HCl.ethanol, 0.6 N HCl, 0.2 N NaOH, 35% NaCl, and Shay' ulcer and acetic acid-induced gastric ulcer. At doses of 500-1000 mg/kg, TKE decreased the gastric secretion and acid output in pylorus-ligation (for 7 h), but 100 mg/kg of TKE had no influence on the gastric secretion. On the other hand, TKE exerted inhibition on the contractile responses of the isolated ileum of mouse to acetylcholine. These results suggested that TKE has an anti-ulcer effect.
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PMID:Anti-ulcer effects of Trichosanthes fruits. 239 55

The healing of acetic acid-induced gastric and duodenal ulcers was examined together with the biochemical indices of growth in gastric and duodenal mucosa in the following three groups of rats: (a) chow-fed, (b) fed an isocaloric liquid diet, (c) fed the liquid diet plus pentagastrin injections (250 micrograms/kg, 3 times/day). Animals received the diet regimen for 10 days from 1 day after induction of ulcer (day 0). Following the feeding regimens, serum gastrin levels, oxyntic gland mucosal DNA synthesis, and gastric secretory function were significantly lowered in the rats fed liquid diets. DNA synthesis in the duodenal mucosa was not different from the pre-ulcer levels. Pentagastrin significantly restored the DNA synthetic and gastric secretory activity of the liquid diet-fed rats toward the levels in the chow-fed group. In the latter group, a significant increase in DNA synthesis and levels of serum gastrin was found at day 6 (after 5 days feeding), which corresponded with a rapid, spontaneous healing of ulcers. Feeding rats liquid diet significantly delayed the healing of gastric, but not duodenal ulcers. Repeated administration of pentagastrin accelerated gastric ulcer healing in the liquid diet group toward the rate observed in the chow-fed group, but had no effect on the healing of duodenal ulcers. These results indicate that cell proliferation is an important factor in the healing of gastric ulcers.
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PMID:Effect of cell proliferation on healing of gastric and duodenal ulcers in rats. 241 90

In an attempt to elucidate the role of granulation vessels in the healing of gastric ulcer, healing and angiogenesis in granulation tissue of acetic acid ulcers were studied in rats. In addition, the effects of prednisolone and synthetic human epidermal growth factor (EGF) on angiogenesis and ulcer healing were investigated. The newly formed granulation vessels in the ulcer base were measured by means of a carmine dye infusion method. Prednisolone, administered subcutaneously at 40 mg/kg/day, significantly decreased angiogenesis in the ulcer base on the 10th day after ulcer production, and on the 30th day ulcer healing was found to be significantly delayed. In contrast, angiogenesis was significantly increased, and ulcer healing was enhanced by intragastric administration of 100 micrograms/kg/day of EGF. With combined administration of prednisolone and EGF, angiogenesis was significantly increased compared to that observed with prednisolone treatment alone. The authors conclude that suppression of angiogenesis by prednisolone is a delaying factor in gastric ulcer healing and that exogenous EGF promotes ulcer healing, partly through restoration of angiogenesis.
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PMID:Effects of prednisolone and human epidermal growth factor on angiogenesis in granulation tissue of gastric ulcer induced by acetic acid. 247 81

Pyrrole aldehydephenyl semicarbazone was shown to be an effective anti-ulcer agent in five experimental models in rats, namely, the indomethacin-induced, acetic acid-induced, pyloric ligation-induced and 0.6 mol HCl, absolute alcohol-induced ulcers, at doses of 40-100 mg/kg. Its anti-ulcer activity and characteristics are similar to those of furazolidone. Its oral acute toxicity in mouse is much lower than furazolidone. This compound exhibited mild inhibitory effects on gastric pepsin secretion, caused increases in hexosamine level and decreases of DNA content in gastric juice. It showed no influence on gastric acid secretion and was considered to have "cytoprotective action" on the gastric mucosa. However, this compound was found to be ineffective against the stress-restraint gastric ulcer model.
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PMID:[The effects of pyrrole aldehydephenyl semicarbazone on experimental gastric peptic ulcer models in rats]. 251 45

The antiulcer effects of OPC-12759, a novel antiulcer agent were compared with those of cetraxate in various experimental ulcer models and on gastric secretion in rats. OPC-12759 (0.3-30 mg/kg, b.i.d., p.o.) significantly accelerated the healing rate of acetic acid-induced gastric ulcer in a dose-dependent manner, while cetraxate did not. When administered orally at 0.3-30 mg/kg, b.i.d., for 7 days, pretreatment with OPC-12759 (0.3-30 mg/kg, b.i.d., p.o.) prevented the formation of acute gastric ulcers, induced by: restraint water immersion stress, aspirin, indomethacin, histamine, serotonin, platelet activating factor (PAF) and DDC. Cetraxate showed antiulcer activity against a part of the OPC-12759-positive gastric ulcer models. Given intraperitoneally at the single dosing range of 10-100 mg/kg, OPC-12759 inhibited the formation of these acute gastric ulcer models. OPC-12759 administered orally at 0.3-30 mg/kg, b.i.d., for 7 days did not inhibit basal gastric secretion in pylorus ligated rats. The results indicated that OPC-12759 possesses wide spectrum antiulcer activity as compared with cetraxate.
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PMID:Effect of OPC-12759, a novel antiulcer agent, on chronic and acute experimental gastric ulcer, and gastric secretion in rats. 254 84

Effects of irsogladine maleate (IM), in combination with histamine H2-receptor antagonists or a muscarinic receptor antagonist, on the formation of stress ulcer were investigated in rats. The ED50 of IM and that of cimetidine for suppressing stress ulceration were remarkably reduced when these drugs were used in combination. ED50s in this case were less than the theoretical values calculated on the basis of additive action, thereby suggesting the synergistic effect of IM and cimetidine. The synergistic effect of IM and ranitidine or famotidine in suppressing stress ulceration was also observed, while IM and pirenzepine did not always produce a synergistic effect. In addition, for acetic acid-induced gastric ulcers, combined administration of IM and cimetidine also markedly potentiated ulcer healing. The marked synergistic potentiation of IM and histamine H2-receptor antagonists may be due to compensatory coordination of both drugs on the gastric secretion and mucosal microcirculation. These results suggest that the combination of IM and histamine H2-receptor antagonists may be beneficial in clinical gastric ulcer therapy.
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PMID:[Synergistic effect of irsogladine maleate and histamine H2-receptor antagonists on experimental gastric ulcers in rats]. 257 21

Glycyrrhetinic acid (Ia) and eighteen related derivatives were examined for antiulcer activity using stress-induced gastric lesions (restraint plus water immersion at 25 degrees C) in mice and rats as screening tests. Among the compounds tested, dihemiphthalate derivatives of 18 alpha- or 18 beta-olean-12-ene-3 beta,30-diol (IV, IIId), 18 beta-olean-9(11)12-diene-3 beta,30-diol (VIc), and olean-11,13(18)-diene-3 beta,30-diol (VIIc) showed potent inhibition of gastric lesion formation at a dose of 12 or 25 mg/kg (p.o.); carbenoxolone sodium (Ib) significantly suppressed the lesion formation at a dose of 500 mg/kg (p.o.). Further evaluation of the antiulcer activity was carried out mainly for compound IIId. Compound IIId (p.o.) prevented the formation of indomethacin-induced or 0.6 N HCl-induced gastric lesions; the latter antiulcer effect was noted even in the combined treatment with indomethacin, suggesting that the effect occurs independently of endogenous prostaglandins. In contrast, compound IIId had no preventive effect against Shay rat ulcer when intragastrically (i.g.) administered; further, no antisecretory effect was seen by i.g. application in pylorus-ligated rats. Administration of compound IIId for 2 weeks accelerated the healing rate of acetic acid-induced gastric ulcer in rats. No significant change in urine excretion was observed after its consecutive administration for 3 d. These results suggest that dihemiphthalate derivatives (IIId, IV, VIc, VIIc) may produce a strong antiulcer activity, probably by strengthening some gastric mucosal defensive mechanism.
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PMID:Antiulcer activities of glycyrrhetinic acid derivatives in experimental gastric lesion models. 260

Effects of zinc in gastric ulcer have been reviewed through investigations carried out on zinc acexamate (ZAC). ZAC is an organic compound that has been shown to possess an experimental antiulcer effect and a wide therapeutic index, making it a useful drug in the treatment of peptic ulcer disease. ZAC protects from ulceration in several experimental models such as pylorus occlusion, reserpine-induced ulcer, necrotizing agents, PAF-induced ulcer and cold-restraint stress. ZAC first reduces the gastric acid output by inhibiting the mast cell degranulation, an action likely to be mediated through a membrane stabilizing action. Secondly, it enhances the mucosal protection factors by increasing mucus secretion, inhibiting the H+ retrodiffusion and improving microcirculation. ZAC is also effective in acetic acid-induced chronic ulcer, restoring the continuity of the damaged mucosa. Several clinical trials have shown the usefulness of ZAC in acute and maintenance treatment of both gastric and duodenal ulcers. Endoscopic studies showed that ZAC reduced the inflammatory processes (gastritis and duodenitis) associated with ulcer healing. This reduction was statistically significant and not observed with other comparative treatments (H2-antagonists). The observed side-effects were minimal and affected less than 2% of treated patients. The pharmacological profile, clinical effectiveness and good tolerance of ZAC suggest this compound as an interesting option in the treatment of peptic disease.
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PMID:Zinc compounds, a new treatment in peptic ulcer. 266 Nov 83

The healing process of acetic acid-induced gastric ulcer in rats was observed with an endoscope for 365 d after ulcer induction. The ulcers were induced by acetic acid solutions of various concentrations (2.5 (I), 5.0 (II), 10 (III) and 20% (IV); 0.05 ml). On day 3, a positive correlation was observed between the ulcer index (UI) and the concentration of acetic acid solution. On day 365, cumulative healing rates in groups I, II, III and IV amounted to 100, 100, 58.3 and 51.7%, respectively. The cumulative relapse rates in groups I, II, III and IV were 0, 13.6, 66.7 and 58.6%, respectively. Significant correlations were observed between initial UI values and cumulative healing or cumulative relapse rate. On day 365, rats were divided into two groups, a healed group and non-healed group, and the gastric mucosal prostaglandin I2 (PGI2) level was measured by bioassay. The PGI2 level around ulcers in ulcer-induced rats was higher than in normal rats, and it was higher in non-healed rats than in healed rats. Moreover, the PGI2 level was higher in those groups which showed a higher cumulative relapse rates. The above results indicated that the initial ulcer size and the PGI2 level around the ulcer might correlate to ulcer healing or exacerbation.
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PMID:Relapse of acetic acid-induced gastric ulcer and gastric mucosal prostaglandin I2 level in rats. 266 61


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