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)

Antacids can reduce gastroduodenal acidity for long periods if taken in substantial quantities after food. Their healing effect on gastric ulcer is minimal, if present at all, and easily overwhelmed by the benefit obtained from admission to hospital. Intensive antacid therapy appears effective in healing duodenal ulcer and preventing haemorrhage from stress ulcer, and is comparable in these respects with cimetidine but with a higher incidence of side-effects. Clinical impression strongly suggests that antacids relieve pain in peptic ulcer but objective confirmation is lacking.
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PMID:Antacids and peptic ulcer--a reappraisal. 3 92

A four year experience in the management of 585 patients with massive upper gastrointestinal tract bleeding (U. G. I. B.)has been reviewed. The effect of routine fiberoptic gastroscopy, selective angiography, and selective pitressin arterial infusion has been analyzed as it effects the more accurate diagnosis and better non-operative therapy of these dangerously ill patients. Duodenal and gastric ulcer, which comprise one-half of such patients, are best treated by early operation. Mallory-Weiss-syndrome is more frequent than previously appreciated. Pitressin infusion is worthy of trial in diffuse gastritis, varicose- and stress ulcer bleeding. Stress bleeding is usually one manifestation of multiple organ failure due to bacterial sepsis.
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PMID:[New methods of managing massive upper gastrointestinal bleedings (author's transl)]. 30 32

Stress and allopurinol (ALL) were investigated in rats with regard to their influence on serum uric acid and glucose concentration, gastric secretion, microcirculation (MBF) and stress ulcer index. There is a non-competitive type of interaction between severe stress and ALL-mediated xanthine oxydase inhibition (= per cent fall in serum uric acid) as compared with control conditions (= mild stress). Vmax is different (84.6 +/- 1.9 and 92.3+/-2.26; P less than 0.05), but not Km (0.39 +/- 0.09 and 0.68 +/- 0.08 mg/kg/h ALL). Serum uric acid is higher in rats with draining gastric fistula than those with closed fistula suggesting that already mild stress is associated with an increase in uricemia in this species. ALL does not significantly alter gastric acid and uric acid secretion but improves markedly gastric ulcer index during mild and severe stress. Since MBF is significantly elevated by ALL during the latter circumstances, a dissociation between MBF and acid secretion is one feature of ALL actions and might become a primary aim in treatment of this disorder.
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PMID:Urate metabolism and gastric ulcerations in rats as influenced by stress and allopurinol. 56 51

Rats were orally administered ascorbic acid at a dose of 30 g/liter during either total starvation, partial starvation, the activity-stress ulcer procedure, or the restraint-cold procedure. In four experiments, ascorbic acid failed to exert significant protective action against stomach ulcer formation and, in fact, may have potentiated the ulcerogenic process.
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PMID:Ascorbic acid and stress ulcer in the rat. 72 47

The aim of the present study was to explore the relationship between depression (helpless withdrawal behavior) and susceptibility to stress ulcer in rats. The WKY genetic strain of rats has been described as highly susceptible to stomach ulcer development during water restraint, i.e., when placed in a jar of water and forced to swim to keep their head above water, a setting in which Richter identified "giving up" behavior akin to hopelessness (Richter, 1957). Since WKY rats tended to float in the water instead of swimming in an attempt to escape, and were also found to be relatively inactive in open field tests, a series of experiments were performed to ascertain whether their diminished activity and their failure to swim reflected slowness, cognitive impairment, or something actually akin to depression. The latter interpretation was supported by evidence from tests of shock avoidance behavior, of capacity to learn discrimination in an operant setting, and by the capacity of an antidepressive drug to lessen floating time in the forced swim test and also to reduce the incidence of stomach ulcers.
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PMID:Learning behavior, escape behavior, and depression in an ulcer susceptible rat strain. 161 Jul 18

Bilateral microinjections of dopamine (DA, 0.3, 3.0 or 30.0 micrograms) or the DA-agonist, bromocriptine (3.0 micrograms) into the basolateral amygdala (BLA) dose-dependently attenuated cold restraint stress (3 h at 4 degrees C)-induced gastric ulcer formation in rats. On the other hand, intra-BLA injections of the neurotoxin, 6-hydroxydopamine (10 micrograms) of the DA-antagonist, haloperidol (0.1 or 1.0 micrograms) aggravated such stress ulcer formation. All these effects were seen only when the injection sites were localized in the posterior (and not the anterior) BLA. Further, pretreatment of rats with haloperidol (0.1 micrograms) clearly antagonized the gastric cytoprotective effects of DA or bromocriptine (both at 3.0 micrograms), when both chemicals were injected in the posterior BLA. The results indicate that DA-ergic mechanisms in the posterior BLA are important for the regulation of gastric mucosal integrity during cold restraint stress.
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PMID:The basolateral amygdala, dopamine and gastric stress ulcer formation in rats. 168 35

Synthetic prostaglandins of the E series have cytoprotective and gastric antisecretory actions. Both actions are relevant to their therapeutic usefulness in treating and preventing gastrointestinal mucosal diseases. Controlled clinical studies have shown prostaglandins to be effective treatment for gastric and duodenal ulcer disease. Although used widely in dozens of foreign countries, however, prostaglandins have not been approved by the United States Food and Drug Administration for use in the treatment of peptic ulcer disease. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with an increased incidence of gastric and duodenal ulcers, gastrointestinal bleeding, and increased morbidity and mortality. Misoprostol, a prostaglandin E1 analogue, is effective in preventing and treating NSAID-induced mucosal damage and has been approved by the Food and Drug Administration for the prevention of NSAID-associated gastric ulcers. Controlled studies have not provided convincing evidence that H2-receptor antagonists or sucralfate prevents NSAID-induced gastric ulcer. Preliminary clinical studies indicate that some E-prostaglandins may also be effective in treating and/or preventing stress ulcer, cystic fibrosis, and hepatorenal syndrome and in improving graft survival in renal transplant patients receiving cyclosporine. Additionally, in vitro and animal studies suggest that prostaglandins may have therapeutic value in inflammatory bowel disease, and they may promote cartilage repair by an inhibitory action on interleukin-1. The latter finding could be of major relevance in preventing cartilage destruction in rheumatic patients. Significant side effects associated with the clinical use of prostaglandins include mild to moderate diarrhea and stimulation of uterine contraction during early pregnancy. Prostaglandins are effective for the treatment of peptic ulcer disease and, to date, are the only effective therapy for preventing the total spectrum of NSAID-induced mucosal damage. These compounds may also prove effective in treating various inflammatory disorders.
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PMID:Prostaglandins: an overview of the worldwide clinical experience. 181 16

The formation of gastric stress ulcers was studied as a function of interactions between thyrotropin releasing hormone (TRH) and endogenous opioids in the central amygdalar nucleus (CEA) in rats. Bilateral microinjections of TRH (1 or 10 micrograms) into the CEA produced dose-related aggravations in cold restraint stress (CRS, 3 h at 4 degrees C)-induced gastric ulcer formation. Similar stress ulcer facilitating effects were also seen with intra-CEA injections of the opioid antagonists, naloxone (1 or 10 micrograms). On the other hand, the enkephalin analog, D-Ala2-metenkephalinamide (DAMEA, 1, 10 or 20 micrograms) produced dose-dependent attenuations in gastric stress pathology, the effects being most marked with the latter two doses. Pretreatment of rats with intra-CEA naloxone (1 microgram) (a) antagonized the gastric cytoprotective effects of DAMEA (20 micrograms) and (b) further aggravated the ulcerogenic response of TRH (1 microgram), without influencing significantly the TRH (10 micrograms) effect. Further, when DAMEA (20 micrograms) was administered intra-CEA just after TRH (10 micrograms), the stress ulcer facilitating effects of the latter was neutralized. The results indicate that TRH-enkephalin interactions are possible at the level of the CEA during CRS-induced gastric ulcer formation.
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PMID:TRH-enkephalin interactions in the amygdaloid complex during gastric stress ulcer formation in rats. 192 93

Bilateral intra-amygdalar (i/am) microinjections of TRH (1 and 10 micrograms) and physostigmine (10 micrograms) into the central nucleus (CEA) aggravated cold restraint stress (3 hr at 4 degrees C) induced gastric ulcer formation in rats, whereas atropine (1, 5 and 10 micrograms) attenuated this phenomenon. Similar stress ulcer reducing effects were seen with chlordiazepoxide (CDP, 10 mg/kg, IP) and midazolam (1, 3 and 10 micrograms, i/am). Pretreatment of rats with atropine or CDP antagonized the ulcerogenic effects of both TRH and physostigmine. Further, when administered intra-CEA, midazolam neutralized the effects of TRH in a dose-related manner. These results are discussed in light of TRH-acetylcholine-benzodiazepine/GABA interactions within the amygdaloid complex during stress ulcer formation.
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PMID:Effects of intra-amygdalar thyrotropin releasing hormone (TRH) and its antagonism by atropine and benzodiazepines during stress ulcer formation in rats. 211 28

The influence of the proximal selective vagotomy (PSV) on the origin and the extent of experimental gastric ulcer were investigated in rats. The lesions of the gastric mucosa were caused in three groups: by stress through swimming-test, by application of phenylbutazone, and by ischemia (ligature of the left gastric and the right gastroepiploic vessels). The PSV practised a protective influence on the pharmacodynamic etiology, however, not on the stress ulcer. The areas of the ischemic gastric ulcers were larger on an average of 40% after PSV than in the control animals. The difference was not statistically significant. In case the PSV caused besides hyposecretion and hypo-acidity even passive hyperemia caused in the denervated part of the stomach then these did not produce any sufficient defence against the origin of stress ulcers and ischemic lesions.
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PMID:[The effect of proximal selective vagotomy on experimental gastric mucosal lesions in the rat]. 222 3


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