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At least 451 records · Page 25Linked to original sources
PubMed2004

The effects of verapamil on stress- and histamine-induced gastric lesions in rats.

The influence of verapamil on stress-induced and histamine-induced gastric ulcers was investigated in rats. The influence of verapamil was also examined on various biochemical parameters that affect the development of these ulcer models. The animals were pretreated with intraperitoneal verapamil (1, 5, 25 mg/kg) by injection 1 h before the induction of experimental ulceration. The gastric lesions were induced by cold-restraint stress or intraperitoneal injection of histamine (300 mg/kg). The gastroprotective effects of verapamil were evaluated by determining the ulcer index, gastric mucus content, free and total acidity, lipid peroxidation and non-protein sulfhydryl content. Verapamil pretreatment at a dose of 25 mg/kg significantly reduced stress-induced ulcers. Verapamil enhanced mucus secretion, reduced total acidity and lipid peroxidation and decreased non-protein sulfhydryl content in a dose-dependent fashion. On the other hand, pretreatment with verapamil at any dose had no significant effect on histamine-induced ulcers. L-Arginine (L-A) (100 mg/kg) or L-nitroarginine (L-NNA) (100 mg/kg) were also injected i.p. to the animals 1 h before stress to test the role of nitric oxide (NO) in the mechanism of the gastroprotective activity of verapamil (25 mg/kg). The results suggested that verapamil stimulates gastric NO production, but the overproduction of NO worsens gastric ulcers. The effects of verapamil on experimentally induced ulcers may be related to its ability to induce biochemical alterations in the parameters measured in gastric tissue.

Animals↗
PubMed2002

Expression of UreI is required for intragastric transit and colonization of gerbil gastric mucosa by Helicobacter pylori.

Helicobacter pylori colonizes the antral mucosa of the human stomach. There is a controversy as to whether the microorganism is exposed to acidity in its ecological niche. In vitro, the microorganism requires urease for gastric colonization and survival at pH < 4.0. UreI encodes an acid activated urea channel enabling urea access to intrabacterial urease at acidic pH. UreI is also necessary for survival at pH < 4.0. However, the role of UreI for both intragastric transit and colonization of the epithelial gastric mucosa has never been analyzed in detail. We therefore infected gerbils, whose intragastric pH and response to infection resemble those of man, with H. pylori G1.1 wild type bacteria and their corresponding isogenic ureI mutants. Inhibitors of gastric acid secretion and colonization were used for manipulation of gastric pH. Gastric colonization was determined by urease assay and PCR. Gastric pH was measured with pH electrodes. Whereas H. pylori wild type or ureI complemented ureI knockout bacteria colonized the antrum, ureI deletion mutants were unable to colonize. However, continuous inhibition of acid secretion resulted in gastric colonization by the ureI mutants, as also observed with the wild type strain. Restoration of acid secretion resulted in eradication of ureI mutants but not wild type bacteria. The data show that ureI is essential for both gastric transit after inoculation and mucosal colonization in the untreated stomach. The eradication of ureI mutants following restoration of acid secretion suggests that the organism is exposed to pH < 4.0 at the surface of the antral mucosa and that UreI provides a target for specific monotherapy of H. pylori infections.

Animals↗
PubMed1977

Gastric secretion and haematological findings in relation to mucosal atrophy after partial gastrectomy.

Twenty-one patients (4 females and 17 males) were re-examined 20 years after partial gastrectomy for benign peptic ulcer. Different stages of morphological change in the gastric stump mucosa were compared with haematological parameters as well as with gastric acid and IF secretions. Biopsy specimens were taken by the direct vision technique. Haematological values including also serum vitamin B12, folate and Schilling test were determined. Gastric acid and IF secretions were lower in all patients with "selective parietal cell atrophy" in the gastric mucosa compared with those of other patients. Serum B12 and Schilling test values showed the same tendency. The present study indicates that it is possible to determine the gastric function dependent on parietal cells according to morphological criteria.

Atrophy↗
PubMed2006

Effect of Mouriri pusa extracts on experimentally induced gastric lesions in rodents: role of endogenous sulfhydryls compounds and nitric oxide in gastroprotection.

Several plants are used in folk medicine to treat gastrointestinal disorders. Mouriri pusa Gardn. (Melastomataceae) is a medicinal plant commonly used in the central region of Brazil against gastric ulcer. Two organic extracts methanolic (MeOH) and dichloromethane (DCM) obtained by sequential extraction from the leaves of Mouriri pusa were evaluated for their ability to protect the gastric mucosa against injuries caused by necrotizing agents (0.3M HCl/60% EtOH, absolute ethanol, non-steroidal anti-inflammatory drug, stress and pylorus ligature) in mice and rats. The best results were obtained after pretreatment with MeOH extract whereas the DCM extract did not show the same significant antiulcerogenic activity. No acute toxicity was observed in animals treated with 5 g/kg, p.o. of MeOH extract. The mechanism involving the antiulcerogenic action of MeOH extract seemed to be related to NO generation and also suggested the effective participation of endogenous sulfhydryl group in the gastroprotective action. Phytochemical investigation of the MeOH extract of Mouriri pusa yielded tannins, flavonoids and (-)-epicatechin. The presence of these phenolic compounds probably would explain the antiulcerogenic effect of the polar extract of Mouriri pusa leaves.

Animals↗
PubMed1980

Aspirin- and taurocholate-induced metabolic damage in mammalian gastric mucosa in vitro.

To clarify the mechanism of initiation of the hydrogen ion backdiffusion, the effects of aspirin and taurocholate, two representative gastric mucosal barrier breakers, on the potential difference, secretory activity, energy metabolism, and the hydrogen ion permeability of guinea pig gastric mucosa was studied in vitro. 1) The ATP content and energy charge of the gastric mucosa showed a statistically significant reduction when the potential difference decreased to one-half of that before addition. 2) The mucosal acid secretion was reduced by addition of the barrier breaker. 3) However, the hydrogen ion backdiffusion, as measured by titrating the acid appearing in the serosal solution, became detectable when the potential difference decreased to one-fourth of that before addition. It has been concluded, therefore, that the primary action of gastric mucosal barrier breakers is to damage the energy metabolism of the mucosal cells, and that the hydrogen ion backdiffusion takes place as the result of cellular death caused by the impairment of energy metabolism.

Adenosine Diphosphate↗
PubMed1991

[Morphological changes in experimental duodenogastric reflux].

The model of a total duodenal-gastric reflux was developed in 20 dogs and morphological changes in the stomach were studied. 5 dogs served as control. Histologic changes occurred 3.5 months and 1 year after the operation were characterized by metachromasia, increased mucus formation, proliferation of epithelial and parietal cells, moderate inflammation. Process of the disease had fluctuations. 6 months after the operation 5 dogs were reoperated for the elimination of reflux and were observed for another 6 months. A complete reversibility of all changes was established. Bacteriological studies showed a considerable increase of bacteria population in the stomach and a pH increase. The authors suggest the term 'reflux gastropathy" to replace the term "alkaline reflux-gastritis".

Animals↗