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

The goal of the work was to evaluate plasma membrane phospholipid composition in rat gastric parietal cells under the histamine H3 receptor activation. The content of cyclic nucleotides was also studied. It was shown that H3-receptor agonist (R)-alpha-methylhistamine increases the phosphatidylcholine (PC) and phosphatidylethanolamine (PE) level and decreases the phoshatidylinositole level in plasma membrane of rat gastric parietal cells and leads to attenuation of the cGMP production and enhancement of the cAMP production under the experimental stress--the induced stomach ulcer formation. The histamine H3-receptor antagonist, thioperamide, insignificantly increases the PC and PE level and increases the phoshatidylinositole level in the plasma membrane of rat gastric parietal cells and leads to cAMP production attenuation, and cGMP contents decreases in the above-stated cells. Thus it was shown that histamine H3 receptor activation causes different effects on polyphosphoinositide and adenylatcyclase cascades in parietal cells under stomach ulcer conditions.
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PMID:[Participation of cyclic nucleotides and phospholipidis in signal transduction of histamin receptor H3 of the gastric mucosa parietal cells in rats with experimental ulcer]. 1633 43

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