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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute treatments with haloperidol (1 mg/kg), clozapine (10 mg/kg) and metoclopramide (10 mg/kg) significantly facilitated cold-restraint-induced gastric ulcer formation in rats. In addition, haloperidol and clozapine also produced gastric mucosal erosions in non-stressed rats. Bilateral lesions of the ventral tegmental area (VTA) and substantia nigra also aggravated stress ulcerogenesis--VTA lesions also being effective in inducing gastric ulcers in non-stressed rats. Long-term treatment with dopaminergic blockers showed variable effects. Clozapine potentiated the gastric stress pathology, whereas no significant facilitation was observed with haloperidol or metoclopramide. In addition, withdrawal from haloperidol did not influence the gastric ulcer formation when compared to controls. The role of central dopaminergic involvement in gastric stress pathology is discussed in light of the present results.
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PMID:Central dopamine systems and gastric stress pathology in rats. 338 89

Gastric ulcerations induced in rats by a combination of indomethacin and cold-stress (5 +/- 1 degrees C) for 6 hr were more severe than those induced by indomethacin or cold-stress alone. The acidity of gastric juice was increased in rats treated with indomethacin plus cold-stressed. Histamine H2 receptor antagonists, (H+-K+) ATPase inhibitors and prostaglandins inhibited gastric ulcer formation in indomethacin plus cold-stress treated rats, whereas anticholinergics aggravated the ulceration. The indomethacin plus cold-stress induced acid secretion was inhibited by cimetidine and omeprazole in pylorus-ligated rats. Atropine had less effect on the increase in acidity than cimetidine and omeprazole. These findings indicate that the ulcer formation in indomethacin plus cold-stress treated rats is related the increased in acidity of gastric juice. This gastric ulcer model may be useful for evaluating antiulcer agents.
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PMID:Effects of indomethacin and cold-stress on gastric acid secretion and ulceration. The effects of anti-acid secretory agents in rats. 367 83

We have previously demonstrated that intracisternal (i.c.) administration of neurotensin (NT), a brain and gastrointestinal tridecapeptide, potently inhibits gastric ulcer formation induced by cold-restraint stress (CRS) in rats. This study evaluated the effect of i.c. NT (17.9 nmol) or vehicle (10 microliter of 0.9% NaCl) on the development of CRS-induced gastric ulcers and on dopamine (DA) concentrations and DA turnover (DOPAC/DA) in selected brain regions after 0, 1, 2 and 3 h of CRS. As anticipated, and in confirmation of previous findings, NT significantly reduced the incidence and severity of CRS gastric ulcers in a time-dependent manner. Neurotensin significantly decreased DA concentration and DA turnover in the striatum. In the nucleus accumbens, however, NT produced a decrease in DA concentration and a concomitant increase in DA turnover after 2 and 3 h of CRS. No significant effects of brain NT on DA concentration and DA turnover were observed in the hypothalamus or olfactory tubercles. These findings suggest that the anti-ulcer effect of brain NT may be mediated, at least in part, by a differential activation of the mesolimbic and nigrostriatal DA systems.
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PMID:Involvement of brain dopamine systems on neurotensin-induced protection against stress gastric lesions. 375 95

This study evaluated the effect of intracisternal (I.C.) administration of the brain and gastrointestinal peptides neurotensin (NT) and bombesin (BOM) on the acute development of gastric ulcers induced by cold-restraint stress (CRS) and ethanol in rats. The results of this study can be summarized as follows: In confirmation of previous observations I.C. NT (30 micrograms) and BOM (1 microgram) significantly reduced gastric ulcer incidence and severity induced by 3h of CRS. The results of the ethanol preparation indicate that although I.C. BOM (1 microgram) significantly (P less than 0.05) increased intraluminal gastric pH and mucus, it did not prevent gastric ulcer formation. NT (30 micrograms), by contrast, was totally inactive in this ethanol model. These findings support a role for brain NT and BOM in protection against psycho-behavioral, but not chemical forms of ulcer-producing stress.
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PMID:Differential effects of intracisternal neurotensin and bombesin on stress- and ethanol-induced gastric ulcers. 376 73

In the years 1980-1983 M. xenopi was isolated from the sputum of 37 persons, 30 of them living in the agglomeration of the regional town in the region of Northern Bohemia with 1,175,000 inhabitants. Only 7 of these 30 had manifestation of pulmonary disease. M. xenopi was found repeatedly in the sputum in 5 patients out of 7 affected and in 2 out of 23 persons who showed no signs of a disease. The prevalence was in males between the age of 52-67 years. All of them suffered from other diseases, as chronic bronchitis, TB healed after lobectomy, lung cancer, fibrotic lung lesions, diabetes mellitus, gastric ulcer healed by resection, chronic alcoholism. Investigations were made for detection of the source of infection. Bacteriological examinations of cold and warm tap water in flats of 9 persons with M. xenopi in their sputa were carried out, as well as cold and warm tap water from flats of 2 healthy persons. M. xenopi was found in tap water of 5 persons with M. xenopi in their sputum and in one of the two healthy persons. In the water of one household we found M. kansasii. We came to the conclusion, that transmission carried out in susceptible persons is most probably due to aerosol during washing and showering with water, containing these mycobacteria.
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PMID:Water-borne Mycobacterium xenopi--a possible cause of pulmonary mycobacteriosis in man. 380 13

Mild stress of restraint for 10 min at an ambient temperature of 18 degrees C increased serum corticosterone levels in rats considerably. Histamine given intravenously prior to restraint alone significantly further intensified the stress-induced elevation of serum corticosterone. Dimaprit and cimetidine failed to modify corticosterone responses to the mild stress. Severe stress of restraint and cold of 3 h duration increased serum corticosterone and free fatty acid levels considerably. Histamine given prior to stress exposure left the corticosterone and hyperlipaemic responses to severe stress unchanged. Dimaprit inhibited and cimetidine intensified the stress-induced hyperlipaemia. The most striking finding in the present experiment was a powerful inhibition of gastric stress ulcer generation by intraventricularly administered histamine. Dimaprit was similarly effective. This strong anti-ulcer effect of histamine was abolished by intraventricular pretreatment of rats with either H1- or H2-receptor antagonists, chloropyramine or cimetidine. The results may suggest that in the rat a mild stress does not fully activate central histaminergic pathways involved in corticosterone responses. During severe stress histamine considerably prevents gastric ulcer generation and both H1- and H2-receptors mediate this action of histamine.
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PMID:The involvement of central histamine receptors in stress-induced responses of serum corticosterone and free fatty acids and in gastric ulcer development. 611 42

Rats were orally administered 1-ascorbic acid, nicotine 1-ascorbic acid and nicotine, or distilled water for 10 days. Following this treatment they were fasted for 24 h and then restrained in a cold environment for 2 h. Nicotine alone produced significantly more gastric ulcers than any other treatment. 1-Ascorbic acid increased ulceration relative to controls. The combined effects of 1-ascorbic acid and nicotine resulted in reduced ulcer incidence and severity. It appears that l-ascorbic acid and nicotine do not act synergistically to augment stress-induced gastric ulcer.
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PMID:Nicotine and ascorbic acid effects on cold-restraint ulcers in rats. 709 99

Antinuclear effects of geranylgeranylacetone (GGA), new acyclic polyisoprenoid, on several types of experimental gastric and duodenal ulcers were studied in rats. The prophylactic administration of GGA (50--200 mg/kg p.o. or 12.5--50 mg/kg i.p.) reduced the gastric ulcers induced by the exposure to cold-restraint stress and by the administration of indomethacin, acetylsalicylic acid (ASA), prednisolone or reserpine and the duodenal ulcer after the administration of cysteamine, although it was not effective against Shay's ulcer. The curative treatment with GGA accelerated the healing process of the gastric ulcers induced by the topical application of acetic acid or thermocautery and by the administration of ASA with the exposure to cold-restraint stress. The antinuclear effect of GGA was more distinct than that of gefarnate in all types of experimental models studied. Carbenoxolone effectively reduced the gastric ulcer formation by cold-restraint stress when it was administered i.p. but not p.o., whereas GGA was effective either i.p. or p.o. GGA and gefarnate did not affect the gastric secretion in pylorus-ligated rats, whereas carbenoxolone definitely reduced the secretion of gastric juice and acid. Hexosamine content in the stomach was reduced by the exposure to cold-restraint stress. The pretreatment with GGA prevented the reduction in hexosamine contents in the superepithelial mucous layer and mucosal layer. These results may suggest a high possibility that GGA is useful for clinical treatment of peptic ulcers, probably through a mechanism of increasing defence force of the gastric mucosa.
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PMID:Antiulcer effect of geranylgeranylacetone, a new acyclic polyisoprenoid on experimentally induced gastric and duodenal ulcers in rats. 719 39

1) One of the possible etiologies of gastric ulcers which frequently occur in the lesser curvature is ischemia or necrosis of the gastric wall, which stem from increased rigidity of the blood vessel walls, mainly caused by dysfunction of sympathetic nerve. 2) The main blood supply to the gastric wall is controlled by gastric arteries, with the gastroepiploic arteries playing only an auxiliary role. 3) It should be noted that gastric bleeding or mucosa necrosis will occasionally occur in some cases of SPV or SV. 4) It was established that experimental rat ulcers of UL-II or UL-III severity which are analogous to human gastric ulcer are produced by cold restricted rat combined with ligation of the gastric arteries (MOHRI's method).
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PMID:New aspects in the pathogenesis of gastric ulcer. 738 52

The influence of various ulcerogenic treatments on healing gastric ulcers induced by thermocautery was studied in mice. A low dose of serotonin (5HT) which did not produce ulceration, was found to aggravate gastric ulcers at 15th or 30th day after thermocauterization, but other ulcerogenic treatments including histamine, norepinephrine, vasopressin, acetic acid ingestion and cold-restraint stress did not affect this induced gastric ulcer. Bleeding and ulceration, however, occurred in the gastric glandular portion in addition to thermocauterization ulcer by the treatment of acetic acid ingestion or cold-restraint stress. Histological sections of gastric ulcers (15th and 30th day) 24 hr after 5HT injection, showed severe necrosis of the regenerated mucosal layer. Microvessel structure in the gastric mucosa as revealed by the Indian-ink infusion, showed a local obstruction of blood flow on the edge of ulcers 1 or 3 hr after 5HT injection. Although acetic acid ingestion increased transmucosal fluxes of Na+ and K+, 5HT had no effect on the ion flux in normal mice. Thus the healed ulcer area was resistant to various ulcerogenic stimulants, except for 5HT, and the vasoactive factor of 5HT may be involved in the aggravating process of gastric ulcers induced by thermocautery.
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PMID:Aggravating effect of serotonin on gastric ulceration induced by thermocautery under the healing process in mice. 745 84


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