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)

Quazolast, a mast cell stabilizer, was evaluated for efficacy against acid independent (alcohol, HCl), or dependent (aspirin, indomethacin) gastric damage in rats. Its gastroprotective profile was compared to that of ranitidine. In addition, the antisecretory and gastric ulcer (acetic acid induced) healing capabilities of these agents were examined. Quazolast, in direct contrast to ranitidine, protected the rat gastric mucosa from acid-independent, but not acid-dependent gastric damage. Quazolast lacked antisecretory activity in rats; however, it did heal acetic acid induced gastric ulcers in this species. On day 15 after acetic acid injection, quazolast significantly healed such ulcers, while ranitidine did not. Although the exact mechanisms of gastroprotection and ulcer healing action for quazolast remain to be determined, it may be an effective agent for the treatment of gastric ulcers.
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PMID:Gastroprotective and ulcer healing profile of the mast cell stabilizer quazolast in rats. 168 5

We have shown previously that acid is one factor, although not the only one, in the pathogenesis of duodenal ulcer pain. In the present study patients with gastric ulcer were endoscoped without sedation or premedication. Under direct vision the ulcer craters were infused sequentially with 0.1 N HCl and normal saline, the sequence of infusion being randomized and double blind. Typical ulcer pain occurred in seven of 19 patients during acid infusion compared with one with saline (p = 0.023). Two patients who developed pain on acid were rechallenged after their pain disappeared, and typical pain recurred in both. Acid therefore has a definite role in the pathogenesis of gastric ulcer pain.
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PMID:Acid and gastric ulcer pain. 147 83

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

A role of epidermal growth factor (EGF) in protection and repair of gastric mucosal injury caused by p.o. administration of 0.6 N HCl was investigated in male Wistar rats. Previous to the study on the role of EGF in gastric mucosal protection and repair, changes of gastric mucosal EGF level was determined sequentially by RIA for 180 min after treatment with 0.6 N HCl and intraperitoneal injection of recombinant hEGF. Concentration of incorporated hEGF into the gastric mucosa reached the peak level at 30 min after injection of hEGF. On the other hand, the gastric endogenous EGF level fell remarkably immediately after treatment with 0.6 N HCl. Successively, an association with the mucosal levels of incorporated hEGF and gastric ulcer indices was investigated in the rats in which hEGF was injected intraperitoneally 30 min prior to or at the same time as oral administration of 0.6 N HCl. In conclusion, pretreatment with hEGF protected significantly against gastric mucosal injury with 0.6 N HCl, whereas simultaneous administration of hEGF could not protect against mucosal injury but indicated possible stimulation of the repair process from acute gastric mucosal damage.
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PMID:Role of epidermal growth factor in protection and repair of gastric mucosal injury. 194 Jan 84

Anatomically, functionally, and clinically, peptic ulcer patients are a heterogeneous group of subjects. These patients can be classified according to the anatomic localization of the niche. The functional state of the gastric mucosa was studied in 30 gastric ulcer patients, 25 duodenal ulcer patients, and 10 normal controls. The classification of the first group was based on Johnson's criteria, with the following results: 10 individuals were type I, 10 were type II, and 10 were type III. Pepsinogen I levels and gastric acid secretion were measured in all 65 subjects under basal conditions and after subcutaneous pentagastrin stimulation. Both basal and stimulated serum pepsinogen I values were significantly higher (p less than 0.05) in gastric ulcer type III patients than in the other four groups. These values in gastric ulcer type I were similar to those of the controls. Gastric ulcer type II patients showed an intermediate functional state similar to that of duodenal ulcer patients. In both gastric ulcer type II and duodenal ulcer patients, the basal and stimulated pepsinogen I levels were significantly higher (p less than 0.05) than those found in controls, whereas the basal serum gastrin levels were similar in the five groups. In conclusion, different HCl and pepsinogen I secretory patterns, with functional heterogenicity of the gastric mucosa, are shown here for the anatomically defined gastric ulcer subsets.
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PMID:Different HCl and pepsinogen I secretion patterns in anatomically defined gastric ulcer subsets. 233 56

Dipyridamole has been studied for its ability to inhibit gastric secretion and to protect gastric mucosa against the injuries caused by hypothermic restraint stress, indomethacin and various necrotizing agents including 80% ethanol, 0.6 M HCl, 0.2 M NaOH and 25% NaCl in rats. The results of this study demonstrate that dipyridamole has both prophylactic and curative effects on various experimentally induced gastric ulcers. It produced inhibition of normal and histamine-stimulated gastric secretion in rats. The intensity of gastric lesions induced by indomethacin and hypothermic restraint stress was reduced significantly by dipyridamole. Our findings also showed that dipyridamole protect gastric wall against hypothermic restraint stress-induced mucus depletion. It produced marked cytoprotective effect against all the necrotizing agents used in this study. The cytoprotective effect of dipyridamole against 80% ethanol was reversed significantly by prior treatment with a dose of indomethacin that inhibits prostaglandin biosynthesis. These data indicate that dipyridamole inhibits the formation of gastric lesions by mucosal generation of prostaglandins. The concentration of nonprotein sulfhydryls were decreased significantly in gastric mucosa after administration of 80% ethanol. Treatment with dipyridamole replenish the reduced level of gastric mucosal nonprotein sulfhydryls, thus suggesting the mediation of its protective effect through sulfhydryls. Our findings show that dipyridamole possesses both antisecretory and antiulcer effects. Further studies are required to determine its role in the prophylaxis and or the treatment of gastric ulcer disease.
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PMID:Gastric antiulcer and cytoprotective effects of dipyridamole in rats. 235 30

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

Lysolecithin has been implicated in the pathogenesis of gastric ulcer and reflux gastritis. By use of canine Heidenhain pouches, we examined effects of lysolecithin on the gastric mucosal barrier both at neutral (PO4 buffer, pH 7) and acidic (0.15 M HCl) pH with respect to interaction of lysolecithin with membrane lipids. At both pH values, 2 mM lysolecithin significantly increased forward diffusion of Na+ and backdiffusion of H+. Both solutions also caused significant efflux of membrane phospholipid and cholesterol. Saturation of neutral and acidic lysolecithin solutions with either lecithin or cholesterol significantly diminished or completely prevented disruption of the barrier to H+ backdiffusion and Na+ forward diffusion. In agreement with other reports, we also demonstrated formation of soluble lysolecithin-lecithin mixed micelles but formation of insoluble lysolecithin-cholesterol complexes. Finally, by use of [3H]polyethylene glycol and [14C]lysolecithin, we demonstrated more rapid mucosal uptake of lysolecithin at acidic than at neutral pH for any given experimental condition. Specifically, mean mucosal uptake of lysolecithin from acidic solutions saturated with lecithin (which did not disrupt the gastric mucosal barrier) was greater than uptake from neutral solutions without added lipid (which did disrupt the barrier). These studies suggest that lysolecithin-lipid interactions play an important role in lysolecithin-induced injury to the gastric mucosa. The most important of these interactions appears to occur in luminal lysolecithin micelles rather than within mucosal membranes.
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PMID:Lysolecithin-lipid interactions in disruption of the canine gastric mucosal barrier. 242 Feb 4

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

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


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