OBJECTIVETo study the precise cause and the specific procedure about gastric mucosal lesion in rats with water immersion-restraint stress(WRS).

METHODSOne hundred and forty-four Wistar rats were divided into 9 groups randomly: A, B, C, D, E, F, G, H and I group. There were 16 rats in each group. A, B and C groups underwent gastric emptying determination. Emptying rate of gastric fluid was determined with radiate nuclide (99m)Tc. D, E and F groups underwent gastric acid secretion determination after cleaning gastric contents and pylorus ligation. G, H and I groups underwent gastric acid secretion determination after pylorus ligation without cleaning gastric contents. Gastric mucosal lesion ulcer index(UI) was evaluated. The relationship between of gastric mucosal lesion and gastric emptying rate and gastric acid secretion were examined.

RESULTSGastric emptying rate decreased obviously when the WRS time was prolonged. There were significant differences among B (WRS 2 h), C group (WRS 4 h) and A group (controlled group) (P<0.01). There was also significant difference between B and C group (P<0.01).The rats' gastric acid secretion was inhibited significantly. The differences among E (WRS 2 h), F (WRS 4 h) and D groups (controlled group) were significant (P<0.01). There was no significant difference between F and E groups (P>0.05). The gastric mucosal lesions were aggravated with time of stress. Gastric contents cleaning could effectively prevent gastric mucosal lesions originated by stress .The operation had no influence on this test. There were significant gastric mucosal lesion UI in B and C groups compared with A group (P<0.01). The difference between B and C group was significant (P<0.01).There were no gastric mucosal lesions in A, D, E, F and G groups. However, There was significant difference between I and F group (P<0.01). No significant difference were found among A, D, E, F and G groups (P>0.05). There were significant difference between H and B group and also between I and C group (P<0.01).

CONCLUSIONSWRS can induce gastric emptying disturbance, reduce gastric acid secretion and cause gastric mucosal lesion. As a factor inducing gastric mucosal lesion, acid can damage gastric mucosa as long as it exists without necessary peracid. The prolongation of acid with gastric mucosa contact period and the decrease of gastric mucosa resistance are perhaps the major causes of gastric mucosal lesion. Besides anti-acid, giving facilitative gastric emptying drugs and gastric lavage during stress ulcer prevention and cure should be considered. Acid evacuation in time is also a major cure for gastritis and recurrent ulcer.

Animals ; Gastric Acid ; secretion ; Gastric Emptying ; Gastric Mucosa ; pathology ; Male ; Rats ; Rats, Wistar ; Stress, Physiological

Ethanol causes mucosal injury to the stomach and which accompanied by back-diffusion of H+. Using several drugs known to modify the gastric acid secretion and to provide cytoprotection the effect of back-diffusion of H+ by ethanol was examined. Following 48 hours of starvation rats were anesthetized with urethane, and their stomachs were filled with 4 ml of 20% ethanol solution containing 1.8 mM HCI (7.2 microEq/4 ml) every 15 min. H+ content of the collected perfusates was determined by back-titration to pH 6.0. The presence of ethanol in the stomach for 1 hour caused a loss of luminal H+ at a rate of 4.8 +/- 0.4 microEq/15 min. Pretreatment of rats with atropine (2 mg/Kg, i.v.), pirenzepine(2 mg/Kg. i.v.), cimetidine (10mg/Kg i.v.), cromolyn sodium (20mg/Kg/hr, i.v.) or domperidone (1 mg/kg. i.v.) did not affect the ethanol-induced H+ back-diffusion. Similarly, no effect was seen in rats treated with prostaglandin E2 (100 microgram/Kg i.v.) or indomethacin (5 mg/Kg, s.c). The addition of procaine (10(-5)~10(-3) M) or propranolol (10(-9)~10(-5) M) to the perfusate did not cause any changes in the ethanolinduced H+ back-diffusion. However, pretreatment of rats with acetazolamide (100 mg/Kg i.v.) or ethoxzolamide(50 mg/Kg/day, p.o. for 6 days), carbonic anhydrase inhibitors, markedly suppressed the ethanol-induced loss of luminal H+. Based on these results, it is suggested that ethanol-induced back-diffusion of H+ is mediated, at least in part, by the activity of carbonic anhydrase, and that cholinergic, histaminergic and dopaminergic mechanisms are not involved. Moreover, the implications of prostaglandins and membrane stability are not suggested.
Absorption ; Animal ; Diffusion ; Ethanol/pharmacology* ; Female ; Gastric Acid/secretion* ; Gastric Mucosa/drug effects* ; Male ; Parasympatholytics/pharmacology ; Protons* ; Rats

AIM AND METHODSBy hydrogen gas clearance technique to measure gastric mucosal blood flow (GMBF) and a high dose of capsaicin to ablate the capsaicin-sensitive afferent fibers, the roles of capsaicin-sensitive afferent fibers and endogenous NO in the gastric acid secretion and hyperemic response to intragastric distention were studied in rats.

RESULTS(1) There was an increase in acid secretion associated with the increase in GMBF to intragastric distention. (2) Pretreatment with a high dose of capsaicin to ablate afferent fibers completely abolished the GMBF and partially inhibited the acid secretion during the intragastric distention. (3) The increase in GMBF to intragastric distention was completely blocked by pretreatment with L-NAME, whereas the acid secretion was significantly attenuated.

CONCLUSIONCapsaicin-sensitive afferent fibers and endogenous NO are involved in the increases of gastric acid secretion and GMBF.

Animals ; Capsaicin ; pharmacology ; Gastric Acid ; secretion ; Gastric Dilatation ; metabolism ; Gastric Juice ; secretion ; Gastric Mucosa ; blood supply ; Male ; NG-Nitroarginine Methyl Ester ; Neurons, Afferent ; drug effects ; Nitric Oxide ; physiology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo evaluate the protective effect of licoflavone on gastric mucosa in rats with chronic superficial gastritis and explore the possible mechanism.

METHODSSD rat models of chronic superficial gastritis was established by intragastric administration of 0.02% ammonia and long-term irregular diet. The rat models were then randomized into model group, vitacoenzyme group and 3 licoflavone groups of high, medium, and low doses. After 30 days of treatment, the gastric histopathology, mucosal lesions, scanning electron microscopy, mucin function production by the gastric mucosa epithelial cells, serum PGE(2) level and gastric microcirculation were assessed to evaluate the protective effect of licoflavone on gastric mucosa.

RESULTSCompared with normal control rats, the rat models of chronic superficial gastritis showed significantly higher gastric mucosal injury rate, histopathological scores and gastric mucin content. Licoflavone significantly ameliorated gastric pathology and increased serum PGE(2) level, enhanced acidic mucin secretion by the epithelial cells, and improved gastric microcirculation in the rat models.

CONCLUSIONLicoflavone feeding suppresses gastric mucosa injury, protects and restores the injured mucosa in rats with chronic superficial gastritis, and these effects are related with the up-regulation of serum PGE(2) level.

Animals ; Chronic Disease ; Dinoprostone ; blood ; Epithelial Cells ; secretion ; Female ; Flavones ; pharmacology ; Gastric Mucosa ; drug effects ; pathology ; Gastritis ; pathology ; Male ; Microcirculation ; Mucins ; secretion ; Rats ; Rats, Sprague-Dawley

Heterotopic gastric mucosa in the upper esophagus is frequently found during endoscopic examination. Although most patients with heterotopic gastric mucosa of the upper esophagus, referred as inlet patch, are asymptomatic, symptomatic patients with complications resulting from this ectopic mucosa have also been reported. Acid secretion by the inlet patch has been suggested in some reports. We report a case of heterotopic gastric mucosa in the upper esophagus, with secretion of acid, demonstrated by continuous ambulatory pH monitoring, and the improvement of pharyngeal symptoms after the use of a proton pump inhibitor.
Adult ; Ambulatory Care ; Anti-Ulcer Agents/administration & dosage ; Case Report ; Choristoma/diagnosis* ; Esophageal Diseases/drug therapy ; Esophageal Diseases/diagnosis* ; Esophagoscopy ; Gastric Acid/secretion* ; Gastric Mucosa/secretion* ; Human ; Hydrogen-Ion Concentration ; Male ; Monitoring, Physiologic/methods ; Prognosis

AIMTo demonstrate the protective effect of nitric oxide (NO) on gastric mucosa and its relationship to the acid secretion of parietal cells under stress in rats.

METHODSWater immersion-restraint stress (WRS) model in SD rats was performed. The gastric mucosal ulcer index (UI), NO contents in gastric mucosa and H+, K(+) -ATPase activity of parietal cells were measured. The effects of N(G)-nitro-L-arginine methyl ester(L-NAME) and L-arginine (L-Arg) on the H+, K(+)-ATPase activity of parietal cells and stress-induced gastric mucosal lesion were observed.

RESULTSL-NAME pretreatment decreased NO contents in gastric mucosa, activated H+, K(+) -ATPase activity of parietal cells and aggravated gastric mucosal lesion, whereas L-Arg pretreatment increased NO contents, inhibited H+, K(+) -ATPase activity and significantly ameliorated stress-induced gastric mucosal lesion.

CONCLUSIONEndogenous nitric oxide plays an important role in protecting gastric mucosa from stress-induced lesion by inhibiting H+, K(+) -ATPase activity of parietal cells.

Animals ; Arginine ; metabolism ; Gastric Acid ; secretion ; Gastric Mucosa ; metabolism ; H(+)-K(+)-Exchanging ATPase ; metabolism ; Male ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Oxidative Stress ; Parietal Cells, Gastric ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stomach Ulcer ; metabolism ; pathology ; Stress, Physiological

AIMThe anti-gastric ulcer constituents from the roots of Crepis napifera (Franch) Babc (Compositae) were studied.

METHODSSolvent partition, Si gel and Rp-18 column chromatography, crystallization and spectral methods were used to extract, isolate and identify two compounds. The activity of compound 1 was tested on the rat stomach by determining the effect on aspirin-induced gastric lesions and on histamine-stimulated gastric acid secretion.

RESULTSTwo sesquiterpene lactone glycosides, taraxinic acid-1'-O-beta-D-glucopyranoside (1) and 11,13-dihydro-taraxinic acid-1'-O-beta-D-glucopyranoside (2) were obtained. Compound 1 at the dose of 80 mg.kg-1 p.o. inhibited significantly the development of aspirin-induced gastric lesions in the rat and at an i.v. dose of 70 mg.kg-1 did not affect histamine-stimulated gastric acid secretion in the lumen-perfused rat stomach.

CONCLUSIONCompound 1 is the active component of the plant which protects gastric mucosa and exhibits anti-gastric ulcer action.

Animals ; Anti-Ulcer Agents ; chemistry ; isolation & purification ; pharmacology ; therapeutic use ; Aspirin ; Crepis ; chemistry ; Disease Models, Animal ; Female ; Gastric Acid ; secretion ; Gastric Mucosa ; secretion ; Male ; Molecular Conformation ; Molecular Structure ; Plant Roots ; chemistry ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Sesquiterpenes ; chemistry ; isolation & purification ; pharmacology ; therapeutic use ; Stomach Ulcer ; chemically induced ; drug therapy

OBJECTIVETo explore the effect of muscovite on the quality of gastric ulcer healing.

METHODGastric ulcers were produced in male rats by serosal application of acetic acid. Rats were gavaged for 14 days with saline, omeprazole and muscovite starting 3 days after ulcer induction. Then the tissue and blood samples were obtained and measured.

RESULTIn the muscovite group, restored mucosa thickness increased, cystically dilated glands decreased, microvessels in connective tissue increased, the secretion of mucus, hexosamine, PGE2, EGF, bFGF were enhanced, and the express of EGFR was stronger.

CONCLUSIONMuscovite can promote the gastric ulcer healing and improve the quality of gastric ulcer healing.

Aluminum Silicates ; pharmacology ; Animals ; Dinoprostone ; blood ; Fibroblast Growth Factor 2 ; metabolism ; Gastric Mucosa ; pathology ; physiopathology ; Hexosamines ; metabolism ; Male ; Materia Medica ; pharmacology ; Mucus ; secretion ; Rats ; Rats, Wistar ; Receptor, Epidermal Growth Factor ; metabolism ; Stomach Ulcer ; chemically induced ; pathology ; physiopathology

OBJECTIVETo investigate the protective effects of the polysaccharides isolated from ganoderma applanatum (PGA) on gastric mucosal injury in rats and the underlying mechanism.

METHODGastric ulcer was induced by either acetic acid or pylorus ligation in the rats. The level of PGE2 and GMBF, and gastric mucus secretion were examined respectively.

RESULTAfter oral administration of PGA (250-1000 mg x kg(-1)) repeatedly, the level of PGE2 and GMBF were obviously increased in gastric mucosa of rats as compared with the model group. The secretions of both free mucus in stomach and mucus of gastric wall were enhanced apparently by PGA in a dose-dependent manner.

CONCLUSIONPGA could strengthen gastric mucosa barrier by improving the level of PGE2, GMBF and the secretion of gastric mucus, which may be one of the mechanisms underlying the protective effect of PGA on the gastric mucosa during the gastric ulcer.

Animals ; Anti-Ulcer Agents ; administration & dosage ; isolation & purification ; pharmacology ; Dinoprostone ; metabolism ; Dose-Response Relationship, Drug ; Female ; Ganoderma ; chemistry ; Gastric Mucosa ; blood supply ; metabolism ; secretion ; Male ; Mucus ; secretion ; Polysaccharides ; administration & dosage ; isolation & purification ; pharmacology ; Rats ; Rats, Wistar ; Regional Blood Flow ; drug effects ; Stomach Ulcer ; metabolism

Menetrier's disease is a rare entity characterized by large, tortuous gastric mucosal folds. The mucosal folds in Menetrier's disease are often most prominent in the body and fundus. Histologically, massive foveolar hyperplasia (hyperplasia of surface and glandular mucous cells) is noted, which replaces most of the chief and parietal cells. Profuse mucus is usually observed during the endoscopy but there have been few cases that show interesting endoscopic findings such as mucus bridge or water pearl. Herein, we report a case of Menetrier's disease showing mucus bridge by excessive mucus observed during the endoscopy.
2-Pyridinylmethylsulfinylbenzimidazoles/therapeutic use ; Amoxicillin/therapeutic use ; Anti-Bacterial Agents/therapeutic use ; Clarithromycin/therapeutic use ; Drug Therapy, Combination ; Gastric Mucosa/*pathology/secretion ; Gastritis, Hypertrophic/*diagnosis/pathology ; Gastroscopy ; Helicobacter Infections/diagnosis/drug therapy ; Helicobacter pylori ; Humans ; Male ; Middle Aged ; Mucus/secretion ; Proton Pump Inhibitors/therapeutic use ; Tomography, X-Ray Computed