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

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

The effects of exposure to an enriched environment on subsequent voluntary ethanol intake and response to restraint stress were examined. Rats at 21 days of age were reared in an enriched environment for 90 days. Non-enriched animals were reared individually in standard laboratory cages. Following an initial 36 day ethanol exposure period, voluntary ethanol (9% v/v) preference was assessed for 10 days. In addition, at the conclusion of the ethanol test session, animals were exposed to restraint stress for a 3 hr period. Results indicate that exposure to an enriched environment produces increased voluntary ethanol consumption as compared to non-enriched controls. Furthermore, animals reared in the enriched environment demonstrated reduced gastric ulcer severity in response to restraint stress. Ethanol per se did not affect ulcer formation.
Alcohol
PMID:The effects of environmental enrichment on voluntary ethanol consumption and stress ulcer formation in rats. 377 45

The current studies were designed to investigate the effect of calcium channel blockers on chemically induced gastric lesions in rats. Results of this study indicate that pretreatment of male F344 rats with the calcium channel blockers verapamil, diltiazem, or Mg2+ significantly protected against ethanol- and indomethacin-induced gastric lesions as demonstrated by gross and histopathologic evaluation. Treatment of rats with calcium channel blockers before ethanol or indomethacin administration resulted in a significant decline in the mean number of lesions per glandular stomach, the damaged area of the glandular stomach, and the severity of lesions. Calcium channel blockers also caused a significant decline in the incidence of indomethacin-induced gastric lesions, but had no effect on the incidence of ethanol-induced gastric lesions. These results offer the first evidence that calcium channel blockers may play an important role in the protection against chemically induced gastric lesions and thereby offer insight into the mechanism of gastric ulcer formation. It is speculated that this knowledge may prove important in the development of new and improved therapies for the treatment and prevention of gastric ulcers in humans.
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PMID:Calcium channel blockers protect against ethanol- and indomethacin-induced gastric lesions in rats. 378 Nov 76

Rats were given 6% ethanol (v/v) as their only source of liquid for 4 days. On the basis of ethanol consumption (g/kg/day), animals were divided into high, medium and low ethanol consuming groups. A non-ethanol exposed control group was also included. Following a 24 hr food deprivation period, animals were restrained for 3 hr. No differences in gastric ulcer frequency or severity were noted with the exception of a slight tendency toward a lower incidence among ethanol consuming rats relative to controls. An unusual observation was the high incidence of duodenal ulcer observed only among ethanol consuming rats. This ethanol-stress interaction is discussed in terms of an animal's history of ethanol exposure.
Alcohol
PMID:Acute ethanol administration: effects on stress-induced gastric and duodenal ulcer in rats. 406 58

Biopsies were taken endoscopically from the fundic, antral, and upper duodenal region of healthy volunteers and gastric ulcer patients and were incubated in carbogen-saturated and buffered Medium 199 at 37 degrees C. The rate of DNA synthesis, estimated as incorporation of tritiated thymidine into tissue DNA, was determined as an index of cellular integrity. During the 30-min incubation, ethanol (25% v/v) significantly (p less than 0.01) depressed DNA synthesis by about 50% in the gastroduodenal mucosa of normal subjects and even by two thirds in the gastric mucosa of gastric ulcer patients. Prostaglandin E2 (PGE2) by itself (1 mg/50 ml) had no stimulatory effect on DNA synthesis; it did, however, reduce the drastic fall in DNA synthesis due to ethanol (p less than 0.005) when administered concomitantly. The basic process underlying cytoprotection by PGE2 in vitro remains to be elucidated. Some indirect mechanisms, such as stimulation of gastric mucosal blood flow, are ruled out by these experiments.
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PMID:Partial prevention of ethanol damage of human gastroduodenal mucosa by prostaglandin E2 in vitro. 620 94

Today, we have effective and potent drugs such as H2-receptor antagonists for the treatment of peptic ulcers. Cimetidine and ranitidine are antisecretory drugs which heal 67-90% of duodenal ulcers in 4 weeks. Certain prostaglandins (PGs) which also heal gastroduodenal ulcers and hemorrhagic gastritis not only diminish gastric acid secretion but also confer unique protective properties on the gastroduodenal mucosa. This phenomenon of 'cytoprotection' is supported by the experimental finding that PGs prevent gastroduodenal mucosal injury caused by absolute ethanol, HCl, NaOH and other irritating agents. Other PGs which do not reduce gastric acid secretion also heal human gastroduodenal ulcers. These special properties of PGs make them potentially beneficial for the treatment of gastric ulcer, and gastroduodenal ulcers accompanying use of nonsteroidal anti-inflammatory drugs as well as hemorrhagic gastritis which is particularly refractory to other therapeutic modalities.
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PMID:Prostaglandins, gastroduodenal ulcer and hemorrhagic gastritis. 633 8

To investigate the hemostatic mechanism of local ethanol injection, ethanol was injected into the gastric mucosa of five adult mongrel dogs and one guinea pig and histologic changes at acute and healing stages were followed. Following a local injection of absolute ethanol, the blood flow in small vessels at the site of injection became instantaneously arrested. Histopathologically, thrombosis of blood vessels in the mucosa and submucosa with edema, predominantly submucosal, was found 10 min after the ethanol injection. There was little or no inflammatory cell infiltration in the injected region. By 4 days after the injection, the base of the formed ulcer became stabilized with a uniform white coating, which, microscopically, was mainly composed of a thick layer of necrotized mucosal tissue. Ethanol showed fixative activity when applied to tissues at concentrations of greater than or equal to 20% although an ethanol concentration of at least 70% was required to accomplish adequate tissue fixation. With 95% or lower concentrations of ethanol, dehydration of tissue was insufficient, and hemostasis due to local vasoconstriction was less conspicuous than with absolute alcohol. Nevertheless, a fixative effect with consequent degeneration and necrosis of cells and secondary thrombosis was evident even at these ethanol concentrations. In patients treated with this hemostatic procedure, exposed blood vessels in the gastric ulcer became necrotized and corroded by fixation with injected absolute ethanol and disappeared from the base of the ulcer within 24 hr as seen in the animals.
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PMID:Endoscopic control of gastrointestinal hemorrhage by local injection of absolute ethanol: a basic assessment of the procedure. 635 77

Most reports of interactions involving analgesics deal with their effects on the actions of other drugs rather than vice versa. Aspirin and ethanol have synergistic effects on the development of gastritis, gastrointestinal bleeding, and chronic gastric ulcer. This must be the most common and most important interaction affecting analgesic toxicity. Combined overdosage of aspirin with central nervous system depressants may be particularly hazardous because suppression of the salicylate-induced respiratory stimulation further shifts the disordered acid-base balance towards acidosis. The toxicity of acetaminophen (paracetamol) depends primarily on the balance between the rate of formation of the hepatotoxic metabolite and the rate of glutathione synthesis in the liver. In animals, prolonged pretreatment with ethanol increases the metabolic activation and acute toxicity of acetaminophen, and there is some evidence that chronic alcoholics are more susceptible to hepatotoxicity following acute overdosage. It has been assumed that this sensitivity in chronic alcoholics is due to microsomal enzyme induction with enhanced metabolic activation of acetaminophen. However, the metabolic activation of acetaminophen, as judged by the urinary excretion of its cysteine and mercapturic acid conjugates, is not increased in heavy drinkers or in patients induced by long-term treatment with anticonvulsants or rifampicin. Microsomal enzyme induction is complex. There are important species differences and different agents may selectively induce different variants of the multiple forms of cytochrome P-450. The acute administration of ethanol greatly reduces the metabolic activation of acetaminophen in heavy drinkers with more than a 50 percent decrease in cysteine and mercapturic acid conjugate production. Thus ingestion of ethanol should reduce the risk of liver damage following acetaminophen overdosage. Cimetidine, which inhibits the oxidative metabolism of some drugs, reduces the hepatotoxicity and increases the dose of acetaminophen in mice required to kill 50 percent of the animals. However, contrary to expectations, cimetidine does not inhibit the oxidative metabolism of acetaminophen in man. Salicylamide competes with acetaminophen for sulphate conjugation but is unlikely to potentiate toxicity following overdosage since sulphate conjugation is rapidly saturated anyway. Animal studies suggest that the hepatotoxicity of acetaminophen after overdosage may be increased by other agents which deplete glutathione, but there is no information on this point in man.
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PMID:Drug interactions affecting analgesic toxicity. 635 60

The effects of prostacyclin (PGI2) and its stable thia-thimo-analogue (Hoe 892) on gastric and intestinal secretions and gastric mucosal lesions have been determined in conscious rats. Both PGI2 and Hoe 892 given subcutaneously (s.c.) reduced dose-dependent gastric acid secretion, the ID50 (dose producing 50% inhibition) being about 48.6 and 11.8 micrograms/kg, respectively. In contrast, intragastric (i.g.) PGI2 and Hoe 892 did not cause any change in gastric acid secretion at doses ranging from 1 to 100 micrograms/kg. Both PGI2 and Hoe 892 reduced significantly intestinal fluid secretion (antienteropooling activity). PGI2 and Hoe 892 given i.g. or s.c. reduced dose-dependent gastric ulcer formation induced by acidified aspirin (ASA), Hoe 892 being somewhat less potent than PGI2. Both PGI2 and Hoe 892 were equally effective against gastric mucosal necrosis induced by absolute ethanol and this effect was observed both after i.g. and s.c. administration of these agents. We conclude that stable thia-imino-PGI2 analogue, Hoe 892, has similar gastric and intestinal antisecretory and protective activity as PGI2 and may be useful in the prevention of gastric damage by various noxious agents.
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PMID:Comparison of gastric and intestinal antisecretory and protective effects of prostacyclin and its stable thia-imino-analogue (Hoe 892) in conscious rats. 639 96

Anti-ulcerogenic effects of trimoprostil, a prostaglandin E2 (PGE2) derivative, were studied in comparison with those of PGE2, cimetidine and sulpiride. Trimoprostil and PGE2 given p.o. prevented the formation of gastric lesions produced by absolute ethanol, 0.2N NaOH, 0.6N HCI and hypertonic NaCl solutions in rats and aspirin-induced fecal occult bleeding in dogs. Although both prostaglandins did not alter the gastric mucus content, they equivalently prevented the stress-induced decrease in the mucus content in rats. The duration of these effects of trimoprostil was longer than those of PGE2. Cimetidine and sulpiride did not exert such cytoprotective effects. Trimoprostil inhibited stress-induced gastric ulcer formation in rats more markedly than PGE2, cimetidine and sulpiride. Trimoprostil and PGE2 at the cytoprotective dose (30 micrograms/kg, p.o.) did not change the gastric blood flow in conscious rats. In Shay rats, trimoprostil at doses larger than the cytoprotective doses inhibited the gastric acid secretion when given p.o., but was not effective when given i.d. PGE2 exerted the similar action, but the potency was clearly weaker than that of trimoprostil. In Heidenhain-pouch dogs, trimoprostil also inhibited the gastric acid secretion stimulated by pentagastrin more markedly than did cimetidine. In conclusion, trimoprostil at doses smaller than the antisecretory doses exerted gastric cytoprotective action with a longer duration than that of PGE2, probably through the preservation of the mucus barrier. Such cytoprotection was not found with cimetidine and sulpiride.
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PMID:[Anti-ulcerogenic and cytoprotective effects of trimoprostil (Ro 21-6937), a trimethylprostaglandin E2 derivative]. 660 97


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