Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori has been implicated in the genesis of human gastritis, dyspepsia, and peptic ulcers. However, its influence in the quality of experimental gastric ulcer healing has not been previously investigated. Standardized gastric fundic ulcers were produced in 50 male Sprague-Dawley rats (150-200 g) by a 4 mm in diameter focal, serosal application of 100% acetic acid. Thirty rats were administered 2 ml H. pylori suspension (urease producing, ATCC 43504) in normal saline (10(8) CFU/ml) 2x/day for 7 days. Twenty rats (controls) received 2 ml normal saline 2x/day for 7 days. Gastric ulcer surface area was measured under a dissecting microscope and mucosal specimens were obtained for qualitative and quantitative histology. No gross or microscopic duodenal abnormalities were identified at sacrifice. Ninety percent of control rats showed grossly and microscopically entirely healed ulcers. The remaining 10% showed partially reepithelialized ulcers (area, 0.78 to 1.77 mm2; mean, 1.27 +/- 0.7 mm2). The grossly "healed" mucosa demonstrated marked dilatation of gastric glands lined with mature surface epithelial cells. Parietal cells were scanty (5-10% of all cells). One hundred percent of the H. pylori-exposed rats showed persistence of chronic active ulcers (area, 1.76 to 19.63 mm2; mean, 8.95 +/- 6.15 mm2). The ulcer beds were infiltrated by acute and chronic inflammatory cells, abundant fibroblasts, and capillary networks. The raised ulcer borders were characterized by dilated glands lined by mature surface epithelial cells. Various special stains demonstrated the presence of H. pylori in the surface mucus and within the crypts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Helicobacter pylori affects the quality of experimental gastric ulcer healing in a new animal model. 174 15

The effects of 2-(E-2-decenoylamino)ethyl 2-(cyclohexylethyl) sulfide (compd. III-1a) on various experimental ulcers were investigated. The oral administration of compd. III-1a at doses ranging from 30 to 300 mg/kg inhibited the acute gastric ulcerations induced by ethanol, HCl.aspirin and indomethacin in rats. Compound III-1a significantly inhibited the water immersion stress-induced gastric ulcer at doses of 3 mg/kg, p.o. The anti-ulcer activity of plaunotol as a reference drug was equivalent on an ethanol-induced ulcer to that of compd. III-1a, but weaker on HCl.aspirin, indomethacin and stress-induced ulcers than that of compd. III-1a. On indomethacin-produced gastric antral ulcer, compd. III-1a showed the same significant inhibitory activity as spizofurone did at a dose of 100 mg/kg, p.o. Compound III-1a also inhibited hemorrhagic shock-, diethyldithiocarbamic acid (DDC)-and platelet activating factor (PAF)-induced ulcers dose-dependently. Plaunotol only showed significant inhibitory activity on PAF-induced ulcer in these three ucler models. The consecutive administration of compd. III-1a (100 mg/kg, p.o.) twice a day significantly accelerated the healing of an acetic acid-induced ulcer and that of plaunotol (200 mg/kg, p.o.) showed the same activity. Moreover, orally administered compd. III-1a at a dose of 100 mg/kg decreased the gastric acid secretion in pylorus-ligated rats. The results in the present study suggest that compd. III-1a has the dual action on ulcer formation.
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PMID:Effects of 2-(E-2-decenoylamino)ethyl 2-(cyclohexylethyl) sulfide on various ulcer models in rats. 177 36

The distribution of (+)-(1R,4aS,10aR)-1,2,3,4,4a,9,10,10a-octahydro-1,4a- dimethyl-7-(1-methylethyl)-6-sulfo-1-phenanthrenecarboxylic acid 6-sodium salt pentahydrate (TA-2711) in stomach was studied after oral administration of 14C-TA-2711 (100 mg/kg) to rats. At 6 h after dosing, most of the radioactivity was found in the lower intestine, caecum and large intestine. However, the radioactivity in the stomach was higher than that in the upper and middle small intestine. The concentration of the radioactivity in the glandular stomach was about 1.5 mg eq. TA-2711/g at 30 min after administration. Thereafter, it decreased gradually to about 60 micrograms eq. TA-2711/g at 6 h after dosing. In the radioluminograms of 6 and 24 h after dosing, most of the radioactivity was observed on the surface of gastric mucosa. After administration to rats with gastric ulcer induced by acetic acid, higher radioactivity was observed in the ulcerated tissues of the stomach than in the nonulcerated control tissues. In the stomach damaged by ethanol, the concentrations of radioactivity in lesion parts were also higher than those in non-lesion parts. In the microautoradiograms of gastric mucosa damaged by ethanol, the developed silver grains were densely distributed in necrotic tissues.
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PMID:Metabolic fate of a new anti-ulcer drug (+)-(1R,4aS,10aR)-1,2,3,4,4a,9,10,10a- octahydro-1,4a-dimethyl-7-(1-methylethyl)-6-sulfo-1- phenanthrenecarboxylic acid 6-sodium salt pentahydrate (TA-2711). II. Distribution in the rat stomach. 177 9

We examined the healing promoting effects of azuletil sodium on acetic acid and clamping cortisone-induced gastric ulcer in rats. For the experiments on clamping-cortisone gastric ulcer, we used not only conventional rats in conventional conditions but also specific pathogen free (SPF) rats on SPF environment in order to prevent infection. The following results were obtained. 1) In acetic acid ulcer, azuletil sodium (AZE) (greater than or equal to 90 mg/kg/day, p.o.) significantly decreased ulcer index. As estimated on the basis of stage analysis (Ulcer, Healing, Scar), AZE (greater than or equal to 30 mg/kg/day, p.o.) significantly promoted the healing of ulcers. 2) In clamping cortisone ulcer (conventional), AZE (100 mg/kg/day, p.o.) significantly promoted the regeneration of blood vessels. 3) In clamping cortisone ulcer (SPF), AZE at greater than or equal to 30 mg/kg/day and 100 mg/kg/day significantly increased the healing index and mucosal regeneration index, respectively. 4) In clamping cortisone ulcer (SPF), the infection that was observed in the conventional test was not seen at all and the acceleration of healing was observed. Furthermore, the extent of adhesion was also reduced, and the standard errors of various healing indices were smaller. From these results, it is concluded that AZE accelerated the healing of experimentally-induced gastric ulcers in rats.
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PMID:[Healing promoting effect of azuletil sodium (KT1-32) on experimental chronic gastric ulcers and acceleration of healing in SPF environment]. 182 59

To clarify the mechanism of gastric ulcer recurrence, we studied acetic acid-induced gastric ulcers. The healing of these gastric ulcers was then studied for 4-21 weeks after the injection. Forty-eight ulcers were examined by macroscopic observation and scanning acoustic microscopy (SAM) and by histologic study of the ulcers. SAM has a higher radio frequency and provides more detailed information about the gastric wall than endoscopic ultrasonography (EUS). Thirteen healed and 35 non-healed gastric ulcers were observed by macroscopic observation over 4-21 weeks. SAM enabled us to observe the normal gastric wall of the rat in five different layers. The SAM echo patterns of the healed ulcers were all one pattern. On the other hand, we were able to classify the echo patterns of the non-healed ulcers into two different patterns; one pattern consisted of a high-echogenic region in the first and second layers with an underlying relatively high echogenic region in a horizontal pattern. The other pattern showed a poorly defined and spotted low-echogenic region in the first and second layers which fanned out toward the fifth layer. However, these two different ulcers could not be distinguished macroscopically. Histologic findings supported the results of the SAM study which showed one pattern in healed ulcers and two patterns in non-healed ulcers. In the non-healed ulcers the two different patterns may be ascribed to the proliferation of collagen fibers. SAM makes it possible to image the proliferation of collagen fibers and identify the two different types with an accuracy of 97%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of acetic acid-induced gastric ulcers in rats by scanning acoustic microscopy. 185 54

In order to elucidate the action of an H2 blocker (cimetidine) and gastric mucosal protection agents (sucralfate and sofalcone) on the relapse and recurrence of gastric ulcer, the effects of cimetidine, sucralfate and sofalcone on the contents of histamine and serotonin and histidine decarboxylase (HDC) activity in the gastric mucosa were examined in the ulcer region and the intact region at the 10th day after the operation to produce acetic acid-induced gastric ulcer in rats. The following results were obtained: 1) HDC activity in the gastric mucosa of rats treated with cimetidine (100 mg/kg twice daily) tended to increase in the intact region, and it was significantly increased in the ulcer region. 2) Increased HDC activity due to cimetidine treatment was observed at the 10th day after interruption of cimetidine administration. 3) The HDC activity in the gastric mucosa was not changed by the treatment with sucralfate (500 mg/kg/day) and sofalcone (200 mg/kg/day). The results suggest that the increased HDC activity in the gastric mucosa might participate in the relapse and recurrence of gastric ulcer after discontinuation of cimetidine administration.
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PMID:[Effects of the anti-ulcer agents on the amine contents and regulating enzyme activity of gastric mucosa during the healing process of acetic acid induced gastric ulcer in rats]. 196 27

The effects of zinc sulphate on gastric ulcer healing rate and mucosal mucus content of acetic acid-induced ulceration in rats have been assessed. Daily treatment with zinc sulphate progressively accelerated ulcer healing in a dose-dependent manner with a significant increase observed on day 15 after ulcer induction in rats treated with 44 and 88 mg kg-1 zinc sulphate. A significant increase in gastric mucosal adherent mucus was also observed in those animals treated with 88 mg kg-1 zinc sulphate. The results suggest that a minimum treatment period of 15 days is needed for the zinc sulphate to be effective, and that zinc ions may promote gastric ulcer healing by enhancing mucus formation to prevent acid back-diffusion into the gastric mucosa.
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PMID:Effect of zinc sulphate on acetic acid-induced gastric ulceration in rats. 198 7

Clonidine 2 mg/kg ig inhibited the rat gastric ulcers induced by pyloric ligation, stress and indomethacin by 71%, 77% and 82%, respectively. Clonidine 2 mg/kg ig tended to accelerate the healing of gastric ulcer induced by acetic acid, and the healing rate was 61%. Clonidine decreased the secretion of gastric acid and pepsin, and increased the release of gastric barrier mucus. These actions may contribute to its protective effect against ulceration.
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PMID:[Effects of clonidine on experimental stomach ulcer in rats]. 213 Jun 4

Zinc sulfadiazine (ZnSD) 50, 100, 200 mg/kg ig inhibited the formation of gastric ulcer induced by indomethacin, stress and pyloric ligation in rats respectively and showed dose-dependently. ZnSD 200 mg/kg ig accelerated the healing of gastric ulcer induced by acetic acid. ZnSD 25 mg/kg ig was effective in preventing ethanol-induced damage of rat gastric mucosa. The amount of gastric mucus glycoprotein in gastric tissues was increased by ZnSD. In general, ZnSD did not influence the volume of gastric juice and pepsin output, but ZnSD 200 mg/kg ig decreased gastric acidity. In vitro, ZnSD also influenced the neutralization of acid. It is suggested that antiulcer action of ZnSD may be related to its preservation of the gastric mucosal barrier and neutralization of acid.
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PMID:[Anti-gastric ulcer activity of zinc sulfadiazine in rats]. 213 Jun 5

The present study was designed to assess histologic and ultrastructural features of gastric mucosa in the areas of grossly healed ulcers (acetic acid-induced gastric ulcers) in rats. The specific question we studied was whether the structure and cellular composition of the gastric mucosa in an area of grossly healed ulcer were fully restored. Eighty Sprague-Dawley rats underwent laparotomy; 100% acetic acid was applied to the lower gastric corpus serosa for 30 s and the abdomen was closed. The stomachs were reopened after 2 weeks or after 2, 3, or 4 months. Standardized gastric wall specimens from the area of grossly healed ulcers were obtained, processed, and evaluated by light microscopy and by transmission electron microscopy. The gastric mucosa of grossly healed ulcers demonstrated re-epithelialization at each study time but the mucosa beneath the surface epithelium displayed prominent histologic and ultrastructural abnormalities. Two different patterns of scar could be distinguished: (a) the mucosa in the area of healed ulcer was thinner (25-45% reduction vs. normal), with increased connective tissue and poor differentiation and/or degenerative changes in the glandular cells; or (b) the mucosa displayed ballooning dilatation of gastric glands, reduction in the microvascular network, and poor differentiation of glandular cells. We conclude that (i) the subepithelial mucosa of grossly healed gastric ulcer displays disorganized restoration of glandular and vascular structures and remains histologically and ultrastructurally abnormal; (ii) these abnormalities may interfere with oxygenation, nutrient supply, and with mucosal resistance and defense, and therefore could be the basis for ulcer recurrence.
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PMID:"Healed" experimental gastric ulcers remain histologically and ultrastructurally abnormal. 221 40


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