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

The effects of a weakly acidic polysaccharide fraction, GL-4, from the leaves of Panax ginseng C. A. Meyer on various experimental gastric ulcer models in mice and rats have been studied. Oral administration of GL-4 at doses of 50 to 200 mg/kg inhibited the formation of the gastric lesions induced by necrotizing agents such as HCl/ethanol and ethanol in a dose-dependent manner. This protective effect was observed not only upon oral but also upon subcutaneous administration of GL-4 (50-100 mg/kg). GL-4 also inhibited the formation of gastric ulcers which were induced by water immersion stress, indomethacin, or pylorus-ligation. The contents of prostaglandin E2 in the gastric juice from rats were not influenced by oral administration of GL-4. The protective action of GL-4 against HCl/ethanol-induced gastric lesions was not abolished by pretreatment with indomethacin. When GL-4 (100 mg/kg, p.o.) was administered into pylorus-ligated rats, both gastric acidity and pepsin activity in the gastric juice decreased significantly.
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PMID:Anti-ulcer activity and mode of action of the polysaccharide fraction from the leaves of Panax ginseng. 147 Jun 67

Gastric ulcer is a multifaceted, pluricausal illness. Knowledge of the pathophysiology of gastric ulcer disease remains incomplete. Current pharmacological management of gastric ulceration is directed primarily at the reduction or neutralization of gastric acid secretion despite evidence that patients with this disease often exhibit normal gastric secretory activity. Attempts have been made to prevent or reduce gastric mucosal injury by cytoprotective agents without diminishing gastric acidity. We review several alternate explanations for the cause of gastric ulcers by examining various experimental models of gastric mucosal damage, including ethanol-, stress-, and nonsteroidal antiinflammatory drug-induced gastric lesions. We also discuss possible new strategies for the treatment of ulcer disease, particularly novel pharmacological targets arising from research conducted with these models. Growing realization that factors other than gastric secretion contribute significantly to the development of gastric ulcer disease prompts the conclusion that these same factors represent viable treatment alternatives.
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PMID:Experimental gastric mucosal injury: laboratory models reveal mechanisms of pathogenesis and new therapeutic strategies. 174 Feb 32

Omeprazole is a specific inhibitor of H+,K(+)-ATPase or 'proton pump' in parietal cells. This enzyme is responsible for the final step in the process of acid secretion; omeprazole blocks acid secretion in response to all stimuli. Single doses produce dose-dependent inhibition with increasing effect over the first few days, reaching a maximum after about 5 days. Doses of omeprazole 20mg daily or greater are able to virtually abolish intragastric acidity in most individuals, although lower doses have a much more variable effect. Omeprazole causes a dose-dependent increase in gastrin levels. Omeprazole must be protected from intragastric acid when given orally, and is therefore administered as encapsulated enteric-coated granules. Absorption can be erratic but is generally rapid, and initially the drug is widely distributed. It is highly protein-bound and extensively metabolised. Its elimination half-life is about 1h but its pharmacological effect lasts much longer, since it is preferentially concentrated in parietal cells where it forms a covalent linkage with H+,K(+)-ATPase, which it irreversibly inhibits. Omeprazole binds to hepatic cytochrome P450 and inhibits oxidative metabolism of some drugs, the most important being phenytoin. Omeprazole has produced short term healing rates superior to the histamine H2-receptor antagonists in duodenal ulcer, gastric ulcer and reflux oesophagitis. It has also been shown to be highly effective in healing ulcers which have failed to respond to H2-receptor antagonists, and has been extremely valuable in treating patients with Zollinger-Ellison syndrome.
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PMID:Clinical pharmacology of omeprazole. 202 1

In a double-blind randomized study, the profile of 24-h intragastric acidity and nocturnal gastric secretion was measured in a group of patients with healed gastric ulcer on placebo and 400 mg cimetidine b.d. and 800 mg nocte. Neither cimetidine regimen significantly decreased daytime intragastric acidity, but the 800 mg nocte dose caused a significant decrease in both nocturnal acidity (18.1 to 5.5 mmol/L; P less than 0.05) and acid output (11.0 to 1.7 mmol 7 h; P less than 0.05). The decrease in nocturnal gastric secretion by 400 mg cimetidine b.d. was not significant. As in duodenal ulcer, 800 mg cimetidine nocte will effectively suppress night-time acid secretion in patients with gastric ulcer while leaving acid secretion during the day unaffected.
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PMID:Twenty-four-hour intragastric acidity and nocturnal gastric secretion in gastric ulcer patients--the effects of cimetidine. 210 90

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

We have investigated the relationship between the suppression of acidity by antisecretory drugs for the treatment of benign gastric ulcer and their corresponding ulcer-healing rates. For a variety of antisecretory drug regimens, there was a significant correlation between suppression of 24-h intragastric acidity and ulcer healing rates after 2, 4 and 8 weeks of treatment. There was a lesser degree of correlation between healing and suppression of nocturnal acidity and the association between suppression of acidity and gastric-ulcer healing rates was less marked than that previously described for duodenal ulcer.
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PMID:The relationship between suppression of acidity and gastric ulcer healing rates. 215 56

The influence of the proximal selective vagotomy (PSV) on the origin and the extent of experimental gastric ulcer were investigated in rats. The lesions of the gastric mucosa were caused in three groups: by stress through swimming-test, by application of phenylbutazone, and by ischemia (ligature of the left gastric and the right gastroepiploic vessels). The PSV practised a protective influence on the pharmacodynamic etiology, however, not on the stress ulcer. The areas of the ischemic gastric ulcers were larger on an average of 40% after PSV than in the control animals. The difference was not statistically significant. In case the PSV caused besides hyposecretion and hypo-acidity even passive hyperemia caused in the denervated part of the stomach then these did not produce any sufficient defence against the origin of stress ulcers and ischemic lesions.
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PMID:[The effect of proximal selective vagotomy on experimental gastric mucosal lesions in the rat]. 222 3

As in duodenal and gastric ulcer patients, a highly significant correlation between suppression of 24-h intragastric acidity and healing rates in reflux oesophagitis patients was demonstrated by meta-analysis of data obtained from the literature (r = 0.90; p less than 0.001). Furthermore, we have demonstrated in eight patients with reflux oesophagitis that 2-week treatment courses with 300 mg ranitidine twice daily and 300 mg four times daily progressively decreased 24-h intraoesophageal acidity but only moderately elevated basal and meal-stimulated serum gastrin concentrations, significantly below gastrin values obtained after a 2-week treatment course with 20mg omeprazole once daily. Further studies are awaited to demonstrate long-term effects on both healing rates and serum gastrin responses with high doses of histamine H2-receptor antagonists.
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PMID:High doses of ranitidine in patients with reflux oesophagitis. 227 68

Rat gastric mucosal blood flow, hydrochloric acid (HC1) secretion, and morphological changes of parietal cells were studied by light and electron microscopy using histochemical techniques. Mucosal blood flow of restrained rats was remarkably decreased compared with that of control rats, whereas the acetylcholinesterase activity, demonstrated by the method of Karnovsky and Roots, was significantly increased especially near the ulcer. In contrast, the differences in volume, acidity and acid output of gastric juice were not significant between control and restrained rats. Hypersecretion of HC1 induced by a parasympathetic stimulant, bethanechol, was inhibited by blood loss or infusion of cytochalasin B, an actin depolymerizing agent. 14C-aminopyrine accumulation in the primary cultured parietal cells was decreased by the treatment with hypoxia and cytochalasin B. These treatments also prevented the increase of 14C-aminopyrine accumulation induced by bethanechol. Actin filaments were evident in the cytoplasm of the parietal cells, particularly around the intracellular canaliculi and beneath the plasma membrane using the FITC-labeled phalloidin reaction and transmission electron microscopic observations of uranyl acetate block stained preparations following heavy meromyosin decorations. Ultrastructural studies of the parietal cells in restrained rats revealed that intracellular canaliculi were dilated with loss of microvilli. Actin filaments were noted to be disassembled, and granular with focal aggregation of actin filaments. Hypoxic vacuoles were also found in the cytoplasm. Treatments with blood loss and cytochalasin B infusion in the in vivo model, and hypoxia and cytochalasin B in the in vitro model, resulted in the similar changes. These observations indicate that actin filaments in the parietal cells of restrained rats may be depolymerized by ischemia. As the result, HC1 secretion would not be enhanced even if the parasympathetic nerves are excessively stimulated in the gastric mucosa. Thus, disturbances of the gastric mucosal microcirculation are considered to be important in the pathogenesis of the stress-induced gastric ulcer.
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PMID:[Studies on the mechanism of restraint-induced gastric ulcer--with special reference to mucosal ischemia and gastric secretion]. 232 29

Any postulate that attempts to explain the aetiology of peptic ulcer must take into consideration a number of established facts. (i) At the beginning of the 20th century there was a steep rise in the incidence of peptic ulcers. Over the past 2 decades, trends have shown a significant decline in some Western countries, such as the United Kingdom, and a significant rise in certain Asian countries, such as Hong Kong and Singapore. (ii) There are marked geographical variations in incidence (for example, it is five times more common in Hong Kong than in Sydney), male: female ratio (for example, 1:1 in USA and 17:1 in India), duodenal ulcer (DU): gastric ulcer (GU) ratio (for example, 0.8:1 in Japan and 32:1 in India), and placebo healing rates. (iii) There is genetic heterogeneity. (iv) A proportion of patients has gastric hyperacidity. (v) Ulcer healing is speeded up by the reduction of gastric acidity, but usually only when the stomach is made relatively hypochlorhydric. (vi) Chronic antral gastritic occurs in 90% of DU and 70% of GU cases. (vii) Ulcer occurs most commonly at the duodenal bulb for DU and at the incisura for GU. No single causative factor can explain these facts, and the aetiology must, therefore, be heterogeneous. Cigarette smoking, ingestion of aspirin and other non-steroidal anti-inflammatory agents and environmental stress are reasonably well-established factors. Current evidence indicates that Campylobacter pylori is causally related to antral gastritis but not to peptic ulcer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peptic ulcer: from epidemiology to cause. 249 56


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