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

Proton pump inhibitors (PPIs) are widely used in clinical practice from early 1990s for the treatment of acid- related diseases. PPIs are superior to histamine2-receptor antagonists or anticholinergic agents. These drugs have proven to be effective, safe and well-tolerated during the past two decades. This brief review presents the pharmacodynamics and pharmacokinetics of PPIs and presents clincal applications of the drugs in acid-related diseases.
Gastric Acid/*secretion ; Gastrointestinal Agents/pharmacokinetics/*pharmacology/therapeutic use ; Humans ; Proton Pumps/*antagonists & inhibitors

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

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

To determine the effect of verapamil on experimental duodenal ulcer, pathologic assessment and secretory study were performed in the rats with ulcerogenic dose of cysteamine. The cysteamine increased gastric acid secretion and produced double duodenal ulcers at the proximal protion of the duodenum. Intramuscular injection of verapamil, 3 hours later, produced a significant decreased in gastric acid secretion which lasted at least 4 hours (cysteamine vs. cysteamine+ verapamil; 63.5 +/- 18.4 muEq vs. 25.5 +/- 9.0 muEq during the 1st hour after verapamil administration, 83.1 +/- 24.2 muEq vs. 27.8 +/- 12.3 muEq during the 2nd hour, 110.9 +/- 14.4 muEq vs. 38.5 +/- 25.9 muEq during the 3rd hour, 116.4 +/- 12.1 muEq vs. 40.7 +/- 29.6 muEq during the 4th hour, p less than 0.001). However, cysteamine-induced duodenal ulcers were not alleviated by two doses of intramuscular verapamil administration (4 mg/kg x 2). It is presumed that suppression of gastric acid secretion may not be sufficient to reduce cysteamine-induced duodenal ulcer formation or that verapamil itself may have aggresive effects against duodenum. To illucidate the exact role of verapamil in cysteamine-induced duodenal ulcer, further studies would be needed.
Animals ; *Cysteamine ; Duodenal Ulcer/chemically induced/*drug therapy/pathology ; Gastric Acid/*secretion ; Injections, Intramuscular ; Male ; Rats ; Rats, Inbred Strains ; Stomach/drug effects/*metabolism ; Verapamil/*therapeutic use

OBJECTIVETo study the long-term results of extended parietal cell vagotomy (EPCV) in the treatment of patients with duodenal ulcer and their complications.

METHODSForm 1979 to 2001, EPCV was performed in 321 patients with duodenal ulcer and their complications. Of these patients 56 had chronic duodenal ulcer, 204 perforation, 16 hemorrhage and 40 stenosis. The following items were evaluated: complications of operation, gastric secretion, gastric emptying, endoscopical and radiographical findings, nutritional status, absorption function, and Visick scale.

RESULTSPostoperative follow-up ranged from 0.5 to 22.0 years (mean 11.3 years) in 289 of the 321 patients with a follow-up rate of 90.0%. Neither operative mortality nor dumping syndrome was noted. Episodic postprandial fullness occurred in 19 patients (6.5%), acid regurgitation in 17 (5.8%) and adhesive ileus in 4 (1.4%). Ulceration recurred in 16 patients (5.5%). Duodenal ulcer was seen in 8 patients (19.5%), hemorrhage in 0 (0%), stenosis in 2 (5.3%), and perforation in 6 (3.1%). Ulcers healed rapidly after medical therapy in 10 patients. Six patients received antrectomy and gastrectomy. In 289 (91.7%) patients of Grade I and II of Visick scale, 191 (95.3%) had perforation.

CONCLUSIONSEPCV is easy to perform with a low rate of post operative complication and ulcer recurrence. It should be a treatment of choice for acute perforation, hemorrhage or stenosis due to duodenal ulcer.

Duodenal Ulcer ; surgery ; Female ; Follow-Up Studies ; Gastric Acid ; secretion ; Gastroscopy ; Humans ; Male ; Peptic Ulcer Perforation ; surgery ; Postoperative Complications ; etiology ; Recurrence ; Vagotomy ; adverse effects ; methods

BACKGROUND/AIMS: Data from previous studies on gastric acid secretion and the prevalence of H. pylori in liver cirrhosis patients remain poorly defined. H. pylori is a potential source of NH3, but the possible role of H. pylori in hepatic encephalopathy is not clear. The purpose of this study was to compare gastric acid secretion, the impact of H. pylori infection, and the production of NH3 between cirrhotic patients and healthy, matched controls. METHODS: Twenty-nine patients with liver cirrhosis (HBV, n=12; Alcohol, n=12; HCV, n=5) were matched with 33 healthy persons for age and sex. None of the patients or controls were being treated with antacids, H2-receptor blockers or proton pump inhibitors. The pH and NH3 concentration was measured in gastric juice obtained by endoscopy. H. pylori infection was diagnosed using the rapid urease test. The level of NH3 in venous blood was also measured. RESULTS: The average gastric pH was significantly higher in cirrhosis patients compared to controls (3.91 vs. 2.99, P<0.05). In addition, the prevalence of hypochlorhydria (defined as pH>4) was significantly greater in cirrhosis patients (45 vs. 21%, P<0.05). In contrast, the prevalence of H. pylori infection (62% vs. 58%) and gastric NH3 concentrations (3.4 vs. 3.3 mM/L) were similar between both groups. However, venous NH3 levels were significantly higher in cirrhotics than in controls (63.1 vs. 25.2 micro M/L, P<0.05). The patients with H. pylori infection had significantly higher gastric NH3 concentration (3.8 vs. 1.6 mM/L) and gastric pH (3.87 vs. 2.76, P<0.05) than those without infection, but no significant difference in venous NH3 levels were detected (39.6 vs. 48.1 micro M/L). In patients with cirrhosis, the presence of H. pylori infection was not correlated with either gastric or blood NH3 levels. CONCLUSIONS: The gastric pH of liver cirrhosis patients is higher than that of controls and a larger proportion of cirrhotic patients have hypochlorhydria. The prevalence of H. pylori in liver cirrhosis patients was similar to that in controls and no correlation was found between gastric and blood NH3 levels. Thus, H. pylori infection does not seem to play a major role in generation of elevated NH3 associated with hepatic encephalopathy.
Achlorhydria/complications ; Ammonia/analysis ; English Abstract ; Female ; Gastric Acid/secretion ; *Gastric Acidity Determination ; Helicobacter Infections/*complications/physiopathology ; *Helicobacter pylori ; Humans ; Hydrogen-Ion Concentration ; Liver Cirrhosis/*metabolism/microbiology/physiopathology ; Male ; Middle Aged

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