Gastric Ulcers In Guinea Pigs Research Articles

Study the effect of Ethanolic extract of Anethum graveolens L. on Aspirin induced Gastric Ulcer in Male Guinea Pigs.

The objective of the present study is to investigate the effect of ethanolic extract of Anethum graveolens L. on Aspirin – induced gastric ulcers in guinea pigs. thirty guinea pigs divided in to five groups (6 each group), first group received oral administration 2ml of normal saline served as negative control. 500mg/kg B.W of Aspirin was used to induced ulcer in guinea pigs for 3 days. after checking for presence of ulcers, the ulcerogenic guinea pigs were divided in to four groups, 2 groups were treated with ethanolic extract of Anethum graveolens L. at doses of (150mg/kg, 300mg/kg) respectively, while a group received cimetidine at dose 20mg/kg for 10days and the last group was the ulcer untreated control (control positive). At the end of the study the animals were sacrificed, the stomach was prepared for estimating, gastric PH , gastric ulcer index, total gastric area, gastric fluid volume, serum MDA and tissue MDA, in addition a gross and histological examination of the stomach. There were significant decrease in PH in control positive , while it showed significant increase(P= 0.05) of gastric ulcer index, total gastric area, gastric fluid volume, serum MDA and tissue MDA compared with the negative control group. The study also revealed significant decrease (P=0.O5) in gastric ulcer index, gastric volume, total gastric area, serum MDA and tissue MDA with a significant increase(P=0.05) in gastric PH in groups treated with ethanolic extract and in the group treated with cimetidine compared with the positive control group. Histological studies showed many pathological changes in stomach ?? control positive group but in the treated with ethanolic extract of Anethum graveolens L at dose 300mg/kg group the histopathological changes near to the normal status, whereas, higher dosage of extract (300mg/kg) was more superior to cimetidine drug in its protection of the stomach

Protective effect of GABA and sodium valproate on stress-induced gastric lesions in guinea-pigs.

gamma-Aminobutyric acid (GABA) and sodium valproate (VPA) inhibit the formation of stress-induced gastric ulcers in guinea-pigs. The present study was conducted to evaluate the effect of these drugs on the development of cold- and restraint-induced gastric ulcers in guinea-pigs. In control saline-pretreated animals, a 3 h exposure to cold and restriction resulted in the production of gastric ulcers in 9 out of 10 animals. GABA (200 mg kg-1 oral, i.p.) completely prevented the development of gastric ulcers. VPA (100 and 200 mg kg-1 i.p.) exerted no significant effects on the development of gastric ulcers. GABA (100 mg kg-1 oral and i.p.) and VPA (oral) also exhibited partially protective activity. It is suggested that GABA may participate in a physiological modulation of the gastric mucosal barrier, by increasing its resistance to stress-induced lesions.

Evaluation of antiulcer and antisecretory potential of Linum usitatissimum fixed oil and possible mechanism of action

The aim of the study was to evaluate the antiulcer activity of Linum usitatissimum fixed oil against aspirin-, indomethacin-, ethanol-, reserpine-, serotonin- and stress-induced gastric ulceration in rats and histamine-induced gastric ulceration in guinea pigs. Attempts were also made to evaluate the in vitro anticholinergic and antihistaminic activity and in vivo antisecretary and antiulcer activity of oil following pylorus ligation in rats. L. usitatissimum fixed oil exhibited significant antiulcer activity against different ulcerogens in experimental animal models. The fixed oil significantly inhibited acetylcholine- and histamine-induced contraction of guinea pig and rat ileums, respectively, suggesting its anticholinergic and antihistaminic activity. The oil also exhibited significant inhibitory effect on gastric secretion/total acidity and aspirin-induced gastric ulceration in pylorus-ligated rats. The lipoxygenase inhibitory, histamine antagonistic and antisecretory (anticholinergic) effects of the oil could probably have contributed towards antiulcer activity. L. usitatissimum fixed oil may be considered to be a drug of natural origin which possesses significant antiulcer activity. The present observation is the first experimental data showing antiulcer activity of L. usitatissimum fixed oil.

Gastric antisecretory and antiulcer activity of oxytocin in rats and guinea pigs

The effect of oxytocin (1 mg/kg s.c) on gastric acid secretion and on different experimentally induced gastric and duodenal ulcers was studied. The acute gastric ulcer models used were pylorus ligation, indomethacin, ethanol and histamine induced acute gastric ulcers. Chronic gastric ulcers were induced using acetic acid and duodenal ulcers by cysteamine hydrochloride. Oxytocin showed significant antisecretory and antiulcer activity in pylorus ligated rats. Similarly oxytocin reduced the ulcer index in histamine induced gastric ulcers in guinea pigs and cysteamine induced duodenal ulcers in rats. The antiulcer and antisecretory effect was comparable to that of ranitidine (50mg/kg, i.p) though less in intensity. However, it did not show any gastric cytoprotective effect in ethanol and indomethacin induced ulcer models but ranitidine showed protection (p<0.05) in later model. Oxytocin enhanced gastric ulcer healing in acetic acid induced chronic gastric ulcer model. The reversal of oxytocin effect by atosiban, an oxytocin receptor antagonist indicates a role for oxytocin receptors. The antiulcer activity of oxytocin can be attributed to its antisecretory effect.

Rapid induction of gastric ulceration in guinea pigs by sequential exposure to a barrier breaker and indomethacin

In short term experiments under halothane anesthesia, guinea pig total gastric pouches were initially and terminally exposed to 0.1 M HCl for 30 min. During an intervening 50-min test period, the gastric mucosa was exposed at pH 7.3, either to a barrier breaker (lysolecithin or diluted bile or sodium taurocholate) or to phosphate buffered saline (PBS) for half of the period, followed by exposure to indomethacin or further PBS for the second half of the test period. Scoring of mucosal damage was assessed from coded photographs and histological slides and by measurement of the transmucosal potential difference. In comparison with controls exposed only to PBS in the test period, indomethacin did produce minor but significant mucosal damage, whereas over this short time interval, the barrier breaking agents did not. Sequential exposure of pouches to lysolecithin and indomethacin caused a highly significant increase in ulceration, compared to controls or to indomethacin or lysolecithin exposure separately.

Effect of histamine and stress on the gastric mucosal Ca2+ content during the development of gastric ulcers.

The influence of histamine, its triazole derivative (3-beta-aminoethyl-1,2,4-triazole) and immobilization stress on the gastric mucosal Ca2+ content during the development of gastric ulcers in guinea pigs and rats was investigated. A considerable fall in the concentration of Ca2+ in gastric tissues of guinea pigs after administration of histamine 0.25 mg/kg, down to 80% (8.0 mumol/g), its derivative (1 mg/kg) to 72% (7.2 mucol/g) and stress to 76% (7.6 mumol/g) was recorded by atomic absorption-spectrophotometric techniques, while the calcium level in the controls stood at 9.9 mumole/g. Similar changes (90-65%) were seen in the blood plasma. In rats, the Ca2+-decreasing effects of stress ran closely parallel with increasing ulceration, and depended on the duration of stress. The immobilization of rats evoked a slight rise in the Na+ content of the gastric tissues. After 4 h immobilization, the tissue concentration of Na+ was increased to 116% of control levels. Cimetidine (100 mumol kg-1 more than 50% inhibited the development of gastric ulcers and prevented the change in Ca2+ concentration ions. Thus, the data suggest that Ca2+ ions take part not only in the regulation of secretion, but also in stress tissue dystrophy.

Prevention of promethazine-induced gastric ulcers in guinea pigs with disodium cromoglycate

The preventive effect of different doses of disodium cromoglycate (DSCG) on promethazine-induced gastric ulceration in guinea pigs was determined. Doses of 12.5 mg/kg of DSCG or higher (up to 200 mg/kg) caused a 35% reduction in promethazine-induced gastric ulceration. The incidence of inhibition of ulcer formation was not dose-dependent. With a dose of 200 mg/kg of cromoglycate alone administered intraperitoneally, gastric ulcers did not occur.

An investigation of antihistaminic activity and gastric ulceration

An investigation of antihistaminic activity and gastric ulceration has been done in guinea pigs and rats. Gastric ulcers were produced in guinea pigs by histamine and restraint procedures, while pyloric-ligation and reserpine were used in rat experiments. Brompheniramine, AHR-224-B, tripelenamine HCl, cyproheptadine HCl and promethazine HCl were effective in preventing histamine-induced ulceration in guinea pigs. Glycopyrrolate, a potent anticholinergic, was ineffective. Brompheniramine, the most potent antihistamine (against histamine-induced ulceration), was further investigated for its effects on gastric ulceration induced by other procedures. In restraint-induced ulcers in guinea pigs, the drug was without protective effect. When the gastric ulceration was produced in rats by pyloric-ligation or reserpine, this antihistamine, in contrast to glycopyrrolate, did not exert a protective action. These studies show that several antihistamines are effective antagonists to histanine-induced gastric ulceration in guinea pigs. The effectiveness of certain pharmacological agents (antihistamine or anticholinergic) in preventing gastric ulceration is determined to a large degree by the method employed to produce the ulceration.

A Comparative in Vivo Study of Antacids II

The in vitro neutralizing power of three commercial antacid tablets was compared with their in vivo antacid action as measured by inhibition of experimentally induced gastric ulcers in guinea pigs. The active or principal active ingredients of the tablets were dihydroxyaluminum sodium carbonate, aluminum hydroxide, and calcium carbonate, respectively.

Development of Gastric Ulcers and Decrease in Reducing Power of Adrenals Following Injection of Bile Salts

Sellards1 reported the development of acute gastric ulcers in guinea pigs following intraperitoneal bile salt injection. His observations have been confirmed and extended by Tashiro and coworkers.2...