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

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

The present experiment demonstrated that relatively high doses of acetazolamide (100 and 200 mg/kg s.c.) induced severe gastric hemorrhagic ulceration in rats. This ulceration was aggravated by oral administration of HC1, but was inhibited by NaHCO3. Further, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were affirmed by an increase in serotonin and histamine released from the stomach after acetazolamide treatment. Acetazolamide injection also increased the protein level, but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increases in serotonin and histamine released may also have been contributing factors for gastric ulcer formation.
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PMID:Pathogenesis of gastric ulceration produced by acetazolamide in rats. 632 41

Gastric ulceration is a complex, multifaceted, pluricausal illness. The pathophysiology of gastric ulcer disease continues to be unclear. The mainstay for pharamacological management of gastric ulceration exists in reduction or neutralization of gastric acid secretion through administration of histamine H2 receptor blockers such as cimetidine and ranitidine. Recent studies show however that the majority of patients experiencing gastric injury exhibit normal or below normal levels of HC1 and pepsin secretion which leaves question to the effectiveness of acid reduction therapy. A viable alternative to H2 receptor blockade is to prevent mucosal injury by maintaining the integrity of the mucosal barrier through administration of prostaglandin analogues. This cytoprotection may reduce gastric damage while maintaining normal acid secretion. Our purpose is to review prostaglandins as a potential therapeutic treatment of gastric and duodenal injury and explore the role of prostaglandins as natural physiological defense mechanisms against gastroduodenal mucosal damage. We also discuss several gastric mucosal damaging agents such as nonsteriodal anti-inflammatory drugs, alcohol, and stress along with comparisons of effectiveness between prostaglandin analogues and H2 receptor blockers in reparation and prevention of injury caused by these agents.
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PMID:Prostaglandins: viable therapy in gastric ulceration. 844 26

We clarified the roles of histamine H(1)-, H(2)-, H(3)-receptors and oxyradicals in the exacerbation of acid-induced gastric haemorrhage and stomach ulcer in endotoxaemic rats by measuring changes in gastric mucosal glutathione concentrations, lipid peroxide generation and histamine levels as well as in luminal electrolytes and haemoglobin contents. Stomach ulcers were evaluated by morphological and histological examination. Rats were deprived of food for 24 h, and challenged intravenously with lipopolysaccharide (LPS, 3 mg/kg) at 0, 12, 18 and 24 h after withdrawal of food. Control rats received saline only. Gastric truncal vagotomy was performed and followed by irrigation for 3 h with an acid solution containing 100 mmol/L HC1 and 54 mmol/L NaCl. The augmentation of mucosal permeability to electrolytes (acid back-diffusion), haemoglobin contents and lipid peroxide levels as well as the lowered mucosal glutathione concentrations were dependent on the duration of LPS intoxication. Serious damage of corpus mucosal cells was observed in acid-perfused stomachs of LPS rats. Intraperitoneal diphenhydramine, an H(1)-receptor antagonist, or ranitidine, an H(2)-receptor blocker, caused dose-dependent inhibition of these ulcerogenic factors. Antioxidants, including ascorbate and sodium benzoate, also were effective in inhibition. Moreover, intraperitoneal R-(alpha)-methylhistamine, an H(3)-receptor agonist, produced elimination, while thioperamide, an H(3)-receptor antagonist, and exogenous histamine elevated mucosal histamine concentrations and haemorrhagic ulcers in LPS rats. It is concluded that gastric haemorrhage and stomach ulcers produced by acid solution in LPS-treated rats are modulated by oxyradicals and histamine H(1)-, H(2)- and H(3)-receptors.
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PMID:Roles of histamine receptors and oxyradicals in aggravation of acid-induced gastric haemorrhagic ulcers in endotoxaemic rats. 1765 30