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)

CD-3400 developed by Nippon Chemiphar Co. Ltd., is a new antihypertensive agent belonging to the class of rauwolfa alkaloids. Influence of the agent on gastric mucosa, healing process of acetic acid-induced gastric ulcer and gastric juice in rats was investigated and compared with effects of reserpine and rescinnamine. CD-3400-induced gastric lesions were fewer in number than those produced with reserpine and rescinnamine in fasted rats. After a three day treatment of CD-3400 to fed rats, however, there were few gastric lesions, while reserpine- and rescinnamine-induced gastric lesions were aggravated to a greater extent that when a single administration was given to fasted rats. Influence of CD-3400, reserpine and rescinnamine on the healing process of acetic acid-induced ulcer was insignificant, but treatment with high doses of reserpine and rescinnamine resulted in death. Pretreatment with CD-3400 and reserpine produced a decrease in gastric acid and K+, and an increase in Na+. Repeated administration of reserpine for 5 days resulted in a decrease of both gastric volume and acid, while such was not seen with CD-3400. Treatment with anticholinergic agents such as atropine sulfate and atropine methylbromide inhibited CD-3400- and reserpine-induced gastric lesions. From these results, it would appear that cholinergic factors play a role in the pathogenesis of CD-3400-induced gastric lesions, as in the case with reserpine, and that the responses of these lesions to reserpine and CD-3400 correlate with changes of ionic fluxes in gastric juice.
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PMID:[Findings in the gastric mucosa and gastric secretion in rats treated with methyl O-(4-hydroxy-3-methoxycinnamoyl)reserpate (CD-3400) and reserpine derivatives]. 1 71

Gastric mucosal erosions were produced in rats by pyloric occlusion and intraperitoneal injection of epinephrine. Gastric ulcer was induced by application of acetic acid to a limited area of the stomach. pH, total amount of acid and volume of gastric juice were determined 5 h after pyloric occlusion. The presence of an acute acetic acid ulcer partly inhibited the development of mucosal erosions induced by pyloric occlusion and epinephrine. The gastric ulcer was associated with decreased acid secretion. A positive correlation was obtained between the degree of mucosal erosions and the total amount of acid in the stomach.
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PMID:Interaction between acute gastric ulcer and epinephrine-induced mucosal erosions in the rat: the significance of gastric acid secretion. 3 36

In order to study the distribution of somatostatin in the upper digestive tract in man, biopsies were taken through endoscopy or at surgery from the fundus, antrum, and duodenal bulb in 15 subjects with no gastroduodenal lesion, 12 patients with severe antral and/or fundic atrophy in the sampling area, 28 patients with an active duodenal ulcer, and 14 patients with a nonmalignant gastric ulcer. The specimens were extracted in 2 N acetic acid and tested for somatostatin content with a specific radioimmunoassay. In the control subjects, the somatostatin concentration (nanograms per milligram of wet weight) was 0.60 +/- 0.12 in the fundus, 1.68 +/- 0.33 in the antrum, and 1.35 +/- 0.30 in the duodenal bulb. Atrophy of the gastric mucosa was associated with a reduction of the somatostatin concentration in the fundus and the antrum. No significant variation was observed in the present series of patients with gastric ulcer. Duodenal ulcer was associated with a reduction of the somatostatin concentration in the antrum (P less than 0.02). These results indicate that somatostatin is widely distributed from fundus to duodenal bulb in adult human subjects, and that lower antral concentrations are observed in patients with duodenal ulcer.
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PMID:Somatostatin in mucosa of stomach and duodenum in gastroduodenal disease. 4 75

An ulcer was induced in the anterior wall of the antrum of cats by local injection of acetic acid solution. Carbonized microspheres, 15 +/- microns in diameter, labelled with 141Ce, 46Sc, and 85Sr, were used to measure blood flow in different regions and layers of the stomach wall. The radioactivity of a blood reference sample and of tissue samples was determined, and the blood flow was calculated for each tissue sample. The blood flow distribution was determined before, 1/2 h, and 1 h after an intravenous infusion of indomethacin in a dose of 3 mg/kg. Two groups of anaesthetized animals were used: animals with a 24-h gastric ulcer and control animals 24 h after laparotomy. In the control animals indomethacin caused a mean reduction in gastric mucosal blood flow of approximately 50%. The flow reduction was about the same in different regions of the stomach. In the muscularis there was no change in blood flow after indomethacin. The blood flow was reduced in the duodenum and jejunum but not in the other intestinal organs studied. The blood pressure and cardiac output remained unchanged. In the ulcer group indomethacin caused about the same reduction in mucosal blood flow. However, the blood flow was reduced less in the ulcer region and tended to increase in the mucosa around the ulcer 1 h after indomethacin infusion.
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PMID:Effect of indomethacin on blood flow distribution in the stomach of cats with acute gastric ulcer. 53 10

An acute, acetic acid induced gastric ulcer in rats is associated with increased capillary permeability and albumin leakage into the gastric wall surrounding the ulcer. This is an inflammatory reaction, and the present experiment was undertaken in an attempt to identify inflammatory mediators in the gastric wall around the ulcer. Rats were pretreated with inflammatory antagonists, and the protein leakage was estimated by means of 125I-labelled albumin 40--60 min and 4 h after ulcer induction. We found no effect on the protein leakage of mepyramine (antihistamine) deseril (antiserotonin) or indomethacin (antiprostaglandin) given separately, or of the combination of mepyramine and deseril. The combination of all three substances, mepyramine, deseril and indomethacin significantly decreased protein leakage at 4 h after ulcer induction. This indicates that prostaglandins are released in the tissues near the acute ulcer. Cimetidine (histamine-H2-antagonist) did not decrease the protein leakage either alone or in combination with mepyramine (histamine-H1-antagonist).
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PMID:Release of inflammatory mediators into the gastric wall of rats with acute acetic acid induced ulcer. 71 Apr 60

An ulcer was induced in the anterior wall of the antrum by local injection of acetic acid solution. Carbonized microspheres 15 +/- 5 micrometer in diameter, labeled with 85Sr and 141Ce, were used to measure blood flow in different regions and layers of the stomach wall, and in each sample the mucosa was separated from the muscularis. The radioactivity of a blood reference sample and the tissue sample was determined, and the blood flow was calculated for each tissue sample. Two groups of anesthetized animals were used: animals with normal stomachs given vasopressin and animals with a 1-week ulcer given vasopressin. The vasopressin was administered intravenously over a 20-min period. In animals with normal stomachs and in animals with a gastric ulcer vasopressin was found to decrease the blood flow to the stomach in all areas examined. The presence of a 1-week ulcer in the cat did not seem to influence the effect of vasopressin.
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PMID:Effect of vasopressin on blood flow distribution in the stomach of cats with gastric ulcer. 72 99

Ulcer was induced in the anterior wall of the antrum by injection of acetic acid solution. Carbonized microspheres 15 +/- 5 mj in diameter and labelled with 85Sr and 141Ce were used to measure blood flow in different regions and layers of the stomach. The radioactivity of the blood and tissue samples was determined, and the blood flow was calculated for each tissue sample. Three groups of anaesthetized animals were used: 1) animals, with normal stomachs, 2) animals with normal stomachs given pentagastrin, 3)animals with a one-week ulcer given pentagastrin. In animals with normal stomachs given pentagastrin during 20 minutes, the mucosal blood flow increased in all areas of the stomach apart from the antrum. In animals with a gastric ulcer pentagastrin was not found to influence the mucosal blood flow significantly. Pentagastrin was not found to change the muscularis flow in animals with normal stomachs, or in animals with a gastric ulcer.
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PMID:Effect of pentagastrin on blood flow distribution in the stomach of cats with gastric ulcer. 83 72

Gastric mucosal erosions were produced in rats by pyloric occlusion and intraperitoneal injection of epinephrine. Gastric ulcer was induced by the application of acetic acid to the anterior wall of the stomach. The gastric lesions were photographed and examined microscopically. 5 h after pyloric occlusion alone, the gastric mucosa looked essentially normal. After pyloric occlusion and injection of epinephrine, superficial mucosal erosions were observed in the major portion of the fundus. The presence of an acute acetic ulcer was found to inhibit partly or completely the development of mucosal erosions usually induced by pyloric occlusion and injection of epinephrine. It is suggested that this might be due to a local release of inflammatory mediators around the ulcer.
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PMID:Interaction between acute gastric ulcer and epinephrine-induced mucosal erosions in the rat. 84 66

The effect of a course-wise introduction of the sperm oil on the intensity of the proteinic synthesis in experimental gastric ulcer was investigated. Tests were conducted on albino male-rats in which an experimental gastric ulcer failing to heal for a long time had been induced through introduction of a 5% acetic acid solution into the subserous membrane of the stomach. The intensity of the proteinic synthesis in the liver and gastric mucosa was assessed by the rate of the glycine-14C and methionine-35S incorporation in the total, mitochondrial and nucleonic proteins on the 7th, 14th, 21st and 28th days of the experimental ulcer course. The sperm oil secured a more effective production and thereby created propicious conditions for an intensified proteinic synthesis. It also contributed to an earlier normalization of the proteinic synthesis rates and to a quicker cicatrization of the ulcerous defect.
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PMID:[Glycine-14C and methionine-35S incorporation into liver and gastric mucosa proteins during sperm oil treatment of experimental stomach ulcer]. 85 60

A chronic gastric ulcer model was produced in rats by the subserosal injection of 20% acetic acid solution (0.015 ml) in order to examine whether (1) acetylsalicylic acid (ASA) irritates the chronic gastric ulcer in active or healed or diminished stage, (2) L-glutamine, given together with ASA, inhibits the adverse effect of ASA. Oral ASA 200 mg/kg/day, given in two divided doses for 10 consecutive days, apparently delayed the healing of the gastric ulcer and irritated the healed ulcer to reulcerate. L-Glutamine, 1,500 mg/kg/day, which was given together with ASA in two divided doses, markedly protected the gastric ulcer both in active and healed stages from the deleterious activity of ASA.
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PMID:Effects of acetylsalicylic acid (ASA), ASA plus L-glutamine and L-glutamine on healing of chronic gastric ulcer in the rat. 95 26


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