Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The aim of the present study was to determine the role of 5-HT3 receptors of the gastroprotective effect of salmon calcitonin (sCT) and sCT-induced changes in gastric, hepatic, brain and brainstem glutathione (GSH) and lipid-peroxidation (LP) levels in rats subjected to cold-immobilization stress. 2. Stress exposure resulted in ulcer formation and a decrease in GSH levels of the liver, brain and brainstem and an increase in gastric and hepatic LP (P < 0.05). 3. sCT prevented stress-induced gastric ulcer development (P < 0.01) and reversed the decrease in hepatic and brain GSH levels (P < 0.05). 4. In the present study, a 5-HT3 receptor antagonist, ICS 205,930 was used. Interestingly, the effect of the blocker on GSH and LP levels of the tissues studied was similar to those of sCT. 5. ICS 205,930 dose dependently reversed the anti-ulcer effect of sCT although it did not antagonize the effect of sCT on GSH and LP levels, but it seemed to show an additive interaction for brain and brainstem GSH and gastric LP levels with sCT.
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PMID:The role of 5-HT3 receptors in the anti-ulcer effect of calcitonin. 772 Oct 34

The spontaneously hypertensive rat (SHR) is a widely used animal model for essential hypertension, and is less susceptible to cold restraint stress in gastric ulcer formation. We previously reported that acid secretion is low in SHR due to sympathetic facilitation compared with normotensive Wistar-Kyoto rats (WKY). The purpose of this study was to evaluate the autonomic nervous function and the gastric mucosal blood flow related to gastric motility during cold restraint stress in SHR. Male SHR and WKY, 24-28 weeks old, were used in this study. Noradrenergic innervation, noradrenaline and dopamine contents in the muscle layer were significantly greater in SHR than in WKY, and tissue choline acetyltransferase activity was significantly lower in SHR. Gastric motility was markedly enhanced by cold restraint stress in WKY. By contrast, SHR maintained the rhythmic and low amplitude contractions regardless of hypothermia. Mucosal blood flow decreased markedly during hypothermia in WKY but was well sustained in SHR. In conclusion, the increase in gastric motility associated with cold restraint stress was suppressed in SHR by sympathetic facilitation in the muscle layer, and this may have contributed to the prevention of ulcer formation by maintaining mucosal blood flow in SHR.
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PMID:Gastric mucosal blood flow in relation to stress-induced hypercontraction in spontaneously hypertensive rats. 776 May 25

The hypothesis that the improvement of neurochemical changes involving the brain dopaminergic and cholinergic systems in aged rats may be related to the their capacity of coping with stress has been investigated by testing the effect of various dopaminergic and cholinergic drugs on stress-induced gastric ulcer development. The model of cold-plus-restraint stress induced gastric lesions has been used in Sprague-Dawley rats aged 24 months, compared to young animals aged 2 months. An increased incidence of gastric ulcers was found in old animals. When these animals were treated with cholinergic or dopaminergic drugs, they showed a higher resistance to stress-induced biological modifications. The most potent drugs were found to be the cholinergic drug, physostigmine and the dopaminergic drug, deprenyl. Furthermore, the induction of hyperprolactinemia by pituitary homografts under the kidney capsule was also accompanied by a reduced incidence of cold-plus-restraint stress induced gastric lesions in aged rats. These results may suggest that the influence of neurotransmitter or hormonal factors on the brain may affect the response of aged rats to the application of physical stress.
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PMID:Neuromediators in aging and gastric mucosal injury. 790 76

Treatment 20 min beforehand with an inhibitor of nitric oxide (NO) synthesis NW-nitro-1-arginine methyl ester (L-NAME) (12.5, 25, 50 or 100 mg/kg, s.c.), dose-dependently intensified gastric glandular mucosal ulceration produced by cold-restraint stress. Hexamethonium (20 mg/kg) or atropine (1 mg/kg) pretreatment s.c. 20 min before stress strongly antagonised stress-evoked ulceration, as well as the ulcer-potentiating effects of L-NAME when either cholinoceptor antagonist was given concurrently with the NO inhibitor. Stress-induced mast cell degranulation was not worsened by L-NAME pretreatment. The findings suggest that NO could confer partial protection against stress-induced gastric ulcer formation; its activity is triggered off by the ulcerogenic mechanism of stress.
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PMID:Nitric oxide inhibition intensifies cold-restraint induced gastric ulcers in rats. 809 77

Experiments were designed to examine whether inhibition of the renin-angiotensin system alters gastric mucosal damage in conscious rats subjected to restraint. Two hours immobilization resulted in an ulcer index of 46 +/- 4 (n = 16) which was decreased by converting enzyme inhibitor (MK 422, enalaprilat) doses of 1 and 10 mg.kg-1.h-1 by 50 +/- 16 (n = 8) and 66 +/- 8% (n = 13), respectively (p < 0.05). Gastric blood flow measured by both the 99Tc-labelled frog erythrocytes and 86Rb-clearance methods was low in untreated rats and increased to more than three-fold in angiotensin converting enzyme inhibitor treated animals. Infusion of saralasin a specific angiotensin II receptor blocker (5 micrograms.kg-1.h-1, n = 25) also decreased the ulcer index by 40 +/- 5% (p < 0.05). Thus inhibition of the renin-angiotensin system in conscious cold-restraint rat increased gastric blood flow and reduced mucosal damage. These results suggest that the renin-angiotensin system plays a significant role in the development of experimental gastric ulcer in the cold-restraint model.
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PMID:Protective effects of the inhibition of the renin-angiotensin system against gastric mucosal lesions induced by cold-restraint in the rat. 817 50

Chronic nicotine treatment worsens stomach mucosal damage by cold (4 degrees C) and restraint (stress): it dose- and time-dependently intensifies stress-evoked gastric glandular ulceration, mast cell degranulation and motility. Nicotine 50 micrograms/ml drinking water, given ad libitum to female Sprague-Dawley rats for 10 days, increases the sensitivity of the isolated stomach strip to acetylcholine-induced contractions; atropine abolishes this action. The isolated anococcygeus muscle from nicotine-treated male rats shows increased sensitivity to noradrenaline-induced contractions, but not to those by acetylcholine. Hexamethonium or atropine pretreatment antagonises stress-induced gastric effects in nicotine-drinking rats. Muscarinic M1- and M2-, but not M3-, receptor block (by pirenzepine, AF-DX 116BS and HHSiD, respectively) inhibits stress ulcer formation in female rats. Although tobacco smoking has been reported to increase free radical formation, mucosal xanthine oxidase which initiates free radical formation is uninfluenced by nicotine; antagonising this enzyme (by allopurinol) or hydroxyl free radical scavenging (by dimethylsulfoxide) does not lessen the effect of nicotine on stress-evoked ulceration. The findings suggest that chronic nicotine treatment produces partial ganglionic blockade of the vagal nerve which leads to muscarinic receptor supersensitivity. This phenomenon contributes significantly to the ulcer-worsening mechanism; muscarinic M1- and M2-receptors appear to be involved. The gastric ulcer-aggravating effect of nicotine in stressed rats appears not to be due to increased free radical formation.
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PMID:Nicotine and gastric ulcers in stress. 829 87

The antiulcer effect of aqueous extracts of the leaves of the neem tree was investigated in rats exposed to 2-h cold-restraint stress or given ethanol orally for 1 h. Extracts were administered in doses of 10, 40, or 160 mg leaf/kg body weight, either as single- or five-dose pretreatment regimens. Neem dose-dependently reduced gastric ulcer severity in rats subjected to stress and also decreased ethanol provoked gastric mucosal damage. The extract appeared to prevent mast cell degranulation and to increase the amount of adherent gastric mucus in stressed animals. These effects may explain, at least in part, the mode of the antiulcer action of neem.
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PMID:The gastric antiulcer effects of the leaves of the neem tree. 831 89

At the turn of the century, duodenal ulcer rose from rarity to affect 10% of males in their life time, subsequently declining in some countries such as UK, levelling off in others such as Germany, and continuing to increase in still others such as Hong Kong. The annual incidence per 1000 population varies from about 1 in Japan to 1.5 in Norway, 1.8 in USA and 2.7 in Scotland, and the frequency also varies within many individual countries, such as Australia, China and India, and among races such as a higher prevalence among whites than blacks in USA and among Chinese than Javanese in Indonesia. Ulcer frequency is higher in winter months, and this appears universal, being true in cold as well as in warm countries. Most places report a rise of ulcer rates among the elderly in recent decades. The male to female ratio also varies geographically, for example from 1:1 in USA to 18:1 in India, and with time such as moving from 2:1 to 1:1 in the last two decades in USA, and the duodenal ulcer to gastric ulcer ratio varies widely from place to place, for example from 0.8 in Japan to 19:1 in Africa and 32:1 in India. Placebo healing rates also differ geographically, ranging from 5% in Philippines to 78% in Mexico. These epidemiological data can only be explained by the presence of multiple aetiological factors, including analgesics, society stress, cigarette smoking, Helicobacter pylori, dietary factors, and genetic factors. Three lines of evidence support a genetic role: family studies, twin studies and blood group studies. Family aggregation occurs more commonly in patients with early-onset (< 30 yr) of symptoms. Blood group O prevalence is more associated with late-onset of symptoms. Other genetic markers include nonsecretor status, HLA antigens, phenylthiocarbamide taste sensitivity, and alpha-1-antitrypsin. Genetic syndromes such as MEN I also support a genetic role and give insight into pathogenetic mechanisms. The best physiological marker is still hyperpepsinogenemia I, which is transmitted by autosomal dominance, despite recent report of lower serum pepsinogen 1 after healing of Helicobacter pylori associated gastritis.
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PMID:Epidemiology and genetics of peptic ulcer. 835 24

Effects of kappa opioid agonist, ketocyclazocine (KCZ) and its antagonist, M(r) 2266, were evaluated on some stress responses in rats. KCZ (1 or 10 mg/kg, ip) dose-dependently attenuated cold restraint stress (CRS)-induced gastric ulcer formation. Similar gastric cytoprotection was also seen with KCZ (1 or 10 micrograms/rat, icv). Pretreatment of rats with M(r) 2266 (0.3 mg/kg, ip) clearly antagonized the ulceroprotective effects of both ip and icv KCZ. KCZ effects on the gastric mucosa during CRS were also reduced by naltrexone (5 mg/kg, ip) pretreatment. KCZ (1 or 10 mg/kg, ip) also attenuated the plasma corticosterone response to CRS and these effects were blocked by M(r) 2266 (0.3 mg/kg) pretreatment. These results indicate kappa opioid receptor involvement during stress reactions and also suggest possible opioidergic interactions during CRS.
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PMID:Role of kappa opioid receptors during stress responsiveness in rats. 838 52

The aim of this study is to investigate the pharmacological effect of the stem bark of Acanthopanax senticosus Harms from Hokkaido (Japanese name: Ezoukogi) in place of the root bark as a restorative tonic on the stress-induced gastric ulcer. In the test, the extract of the stem bark of A. senticosus prepared with hot water was dissolved in water and used for the assay of the protective effect of gastric ulcer (erosion) on stressed rats that were restrained on cold water. The result from a single oral administration of the stem bark of A. senticosus-extract (50, 100 and 500 mg/kg, per day) dissolved in 1 ml distilled water did not show any protective effect on gastric ulcer, but the protective effect was observed in a dose-dependent manner from the oral administration of the extract (50, 100 and 500 mg/kg, per day) for 2 weeks. Pre-administration of the stem bark of A. senticosus-extract in a dose of 500 mg/kg showed the most potent inhibition without affecting either body or adrenal glands weights. Among ether, chloroform, n-butanol and aqueous residue extracts from the stem bark of A. senticosus-extract, the n-butanol extract used for oral administration for 2 weeks showed an obvious inhibition of 61.1% on gastric ulcer, compared with the control group which was treated with distilled water in the same way. Chlorogenic acid and syringaresinol di-o-beta-D-glucoside, as the major components of the n-butanol extract, showed a significantly inhibitory effect on gastric ulcer, at 21.4% and 51.3%, respectively. We suggested that the protective effect of the stem bark of A. senticosus on gastric ulcer may be partially due to those of chlorogenic acid and syringaresinol di-o-beta-D-glucoside.
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PMID:Protective effects of Acanthopanax senticosus Harms from Hokkaido and its components on gastric ulcer in restrained cold water stressed rats. 888 47


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