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)

The prostaglandins E2 and 16,16-dimethyl-PGE2 methyl ester were compared with the H2-receptor antagonists burimamide and metiamide for their effects on gastric acid secretion (GAS) and gastric mucosal blood flow (MBF) in rats and dogs, and on ulcer formation in rats. Orally, both 16,16-dimethyl-PGE2 methyl ester (20 microgram/kg) and metiamide (6 mg/kg) were markedly effective inhibitors of GAS stimulated by histamine acid phosphate or pentagastrin in Heidenhain pouch dogs, producing a reduction both in volume of gastric juice and in the concentration of titratable acid. In anaesthetised rats, however, the H2-receptor antagonists, when perfused into the gastric lumen, did not consistently inhibit the increased GAS caused by various secretagogues. In contrast, the prostaglandins, under the same conditions, caused marked inhibition of GAS provoked by all secretagogues. Intravenously, both burimamide and metiamide were effective in inhibiting GAS in rats but were less potent than the prostaglandins. The order of potency was: 16,16-dimethyl-PGE2 methyl ester greater than PGE2 greater than metiamide greater than burimamide. By the oral route, the H2-receptor antagonists were found to be very weak inhibitors of indometacin-induced gastric ulcer in rats, as compared to the prostaglandins. MBF studies in rats and in Heidenhain dogs showed that i.v. or p.o. administration inhibited both GAS and MBF in most cases. The ratio r = [MBF (ml/min)/GAS (mumol H+/min)] was generally increased by both types of compounds, suggesting a preferential effect on GAS.
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PMID:A comparative study of the effects of prostaglandins and H2-receptor antagonists on gastric acid secretion, mucosal blood flow and ulcer formation. 3 81

The preventive effects of hydroxychalcone derivatives on ulcer formation induced by severe necrotizing agents such as 60% ethanol in 150 mM HCl (HCl-ethanol) and 0.2 N NaOH in rats were examined. Among the compounds tested, 2',4'-dihydroxychalcone gave the strongest activity in both experimental models and protected the gastric mucosa from the insult of either necrotizing agent at oral doses ranging from 1 to 10 mg/kg, as evidenced by a dose-related reduction in the ulcer index. The mucosal protective activity of 2',4'-dihydroxychalcone was not affected by pretreatment with indomethacin (5 mg/kg, s.c.). To investigate the detailed mechanism of the mucosal protective action of 2',4'-dihydroxychalcone, its inhibitory effects on the decrease in the hexosamine content from the gastric mucus induced by HCl-ethanol were studied by using it in combination with a dye, Alcian blue. As a result, 2',4'-dihydroxychalcone at an oral dose of 10 mg/kg inhibited the decrease in the dye-recovery from the gastric mucus induced by HCl-ethanol. PGE2 at an oral dose of 0.1 mg/kg exhibited a similar action. These results established that 2',4'-dihydroxychalcone is a potent cytoprotective agent similar to PGE2 effectively preventing gastric ulcer formation induced by strong necrotizing agents and seems to suggest that this compound protects the stomach against its own peptic secretions by reinforcement of gastric resistances. In fact, 2',4'-dihydroxychalcone prevented ulcer formation induced by water-immersion stress in rats and also showed a marked enhancement of the healing of acetic acid-induced gastric ulcers in rats.
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PMID:Gastric cytoprotective anti-ulcerogenic actions of hydroxychalcones in rats. 147 Jun 60

It is widely accepted that patients with aortic aneurysm (AA) show a higher incidence of peptic ulcers than those without. However, the pathogenesis of peptic ulcers associated with AA remains obscure. We measured the gastric mucosal blood flow (GMBF) endoscopically and also determined the gastric mucosal prostaglandin (PG) levels of these AA patients to investigated the mechanism behind gastric ulcer formation. Moreover, we investigated the consumption coagulopathy (CC) of AA responsible for inducing the hemorrhage from ulcers. The GMBF values of 7 AA cases, taken at the antrum, angle and corpus, were significantly decreased compared with those of control cases, while the PGE2 levels of the gastric mucosa were also significantly reduced. With regard to CC, the serum levels of fibrinogen or platelets were significantly lower than those of the control group. These results indicate that the decrease in GMBF, followed by the reduction in endogenous PG, might contribute to the gastric ulcer formation in AA patients, and that CC associated with AA could be an important factor causing the hemorrhage from these ulcers. AA patients should therefore be treated with focusing attention on the possibility of an associated ulcer and ulcer bleeding.
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PMID:The formation of gastric ulcers with a tendency to hemorrhage in association with aortic aneurysms. 185 31

The effect of somatostatin-14 (SST), at doses utilized in clinical practice, on gastric intraluminal prostaglandin (PG) E2 release was evaluated in 8 endoscopically normal subjects, in 6 patients with benign gastric ulcer and in 8 patients with gastric adenocarcinoma. In normal subjects, SST induced a significant increase in gastric intraluminal PGE2 concentration and output, whereas it did not augment the concentration and output of PGE2 in patients with gastric ulcer and with gastric cancer. The altered PG response to SST stimulation shown by gastric ulcer and gastric cancer patients may be related to a modified cell population in the gastric mucosa and/or to a defective regulation of this local gastric mucosal mediator.
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PMID:Basal and somatostatin-stimulated gastric intraluminal prostaglandin E2 in patients with gastric ulcer and with gastric adenocarcinoma. 197 75

PGE2-like immunoactivity was measured radioimmunologically in specimens from gastric corpus mucosa in (a) healthy subjects, (b) patients without liver disease in the absence or presence of gastric ulcer, and (c) patients with alcoholic cirrhosis in the absence or presence of gastric ulcer, further divided into subgroups without or with portal hypertension. The PGE2-like immunoactivity was almost the same in subjects without liver disease and in cirrhotic patients without portal hypertension. A significantly decreased PGE2-like immunoactivity was found in patients with portal hypertension, especially in cases of congestion in the mucosa. A further decrease of the PGE2-like immunoactivity could be found whenever gastric corpus ulcer was present. This decrease is statistically significant. We therefore concluded that a decrease in the PGE2-like immunoactivity in the gastric mucosa of cirrhotic patients is closely related to portal hypertension. Congestion in the mucosa, thought to be a relevant factor in the pathogenesis of the mucosal PGE2 deficiency, might also play a role.
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PMID:Decreased prostaglandin E2 immunoactivity of gastric mucosa in portal hypertension. 203 Aug 9

Investigations were carried out as to whether a disturbance in the formation of cytoprotective prostaglandin (PG) E2 in gastric mucosa is implicated in chronic renal failure. PGE2-like immunoactivity in gastric mucosal specimens was measured in individuals with chronic renal failure (creatine clearance less than 10 ml/min), in individuals without any renal disease, presenting either gastric ulceration or not, as well as in healthy subjects. Regardless of the group of patients, compared to normal mucosa a significant decrease in PGE2-like immunoactivity (about 50-70%) was found in mucosa from atrophic gastritis but not from superficial gastritis. Whenever patients of the control group or patients with kidney disease suffered from ulcers, PGE2-like immunoactivity showed a decrease of about 60-70% in the non-ulcerated mucosa compared to that of non-ulcer subjects. Moreover, ulcer patients showed the same frequency of gastritis and similar mucosal PGE2-like immunoactivity in their non-ulcerated mucosa. Furthermore, compared to the tissue from the ulcer edge, independent of the presence of renal disease, a relative deficiency of PGE2-like immunoactivity of about 50-60% was detected in the non-ulcerated mucosa of ulcer patients. We therefore conclude that chronic renal failure probably has no impact on PGE2 formation in the gastric mucosa. All told, relative mucosal PGE2 deficiency in gastric ulcer disease seems not to be correlated with chronic renal failure.
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PMID:Gastric mucosal prostaglandin E2 levels in gastric non-ulcer and ulcer patients with chronic renal failure or without renal disease, and in healthy subjects. 207 10

Gastric ulcers in children are often seen as a result of an imbalance between nocive factors and the resistance of the mucosa. Glanzmann's thromboastenia is a defect in platelet aggregation and its nature may be associated to local factors which precipitate or perpetuate bleeding. Prostaglandins are hormones of local action which inhibit the secretion of acid and therefore protect the mucosa. We report a case of an 18 year old male youngster with Glanzmann's thromboastenia and a gastric ulcer previously unsuccessfully treated with cimetidine, aluminum hydroxide solution, ranitidine, sucralfate and later controlled with PGE2. In sum, the usefulness of the cytoprotecting effects of the prostaglandins are successfully evaluated in a young man with platelet aggregation abnormalities.
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PMID:[Chronic gastric ulcer in a child with Glanzmann thrombasthenia. Usefulness of prostaglandin E2]. 212 26

PGE2-like immunoactivity in mucosal specimens from gastric corpus and antrum was measured in individuals with chronic uremia or without renal diseases in absence or presence of gastric ulcerations and in healthy subjects. Regardless the group of patients, compared to normal mucosa, a significant decrease in PGE2-like immunoactivity (50-70%) was found in mucosa from atrophic, but not from superficial gastritis. Whenever patients of the control group or patients with renal diseases suffered from ulcers, PGE2-like immunoactivity, compared to nonulcer subjects, revealed a decrease of about 60-70% in the nonulcerated mucosa. Compared to nonulcerated mucosa, the tissue of the ulcer rim in all patients with gastric ulcer showed a relative increase in PGE2-like immunoactivity, eg, PGE2-like immunoactivity was twice as high in tissue from the ulcer rim. The output of PGE2-like immunoactivity into the gastric juice of subjects without renal diseases was comparable to that found in patients with chronic uremia in both basal and pentagastrin-stimulated conditions. We therefore conclude that gastric mucosal formation is probably not influenced by chronic uremia.
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PMID:Gastric mucosal PGE2 levels in gastric non-ulcer and ulcer patients with chronic renal failure or without renal diseases and in healthy subjects. 225 34

The present study investigated the preventive and curative effects of prostaglandins (PGs) on gastric ulcer in rats induced by physical or psychological stresses; some rats were electrically shocked, while others were exposed to affective stimuli arising from the shocked animals. The synthetic PGs dimethyl-PGE2 and rioprostil were administered orally, and their preventive effect on gastric ulceration was evaluated by determining the incidence and the ulcer index of lesions. The curative effect of drugs on ulcer healing was evaluated by determining a time-dependent change in the mucosal surface of the stomach with an endoscopic technique. Oral administration of dimethyl-PGE2 or rioprostil (25 and 50 micrograms/kg) prevented gastric ulceration significantly. Oral administration of these drugs (50 micrograms/kg, twice per day) significantly promoted the healing process of lesions 24 and 36 hr after termination of stress loading. The present results give direct evidence of the curative effect of PGs on stress ulcers and suggest that application of the endoscopic technique to the pathology of the rat's stomach may be a substantial aid in the preclinical evaluation of antiulcer drugs.
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PMID:Preventive and curative effects of prostaglandins on stress ulcer in rats. Application of endoscopic observation. 249 67

The TXA2/PGH2 receptor antagonistic activity of azuletil sodium (KT1-32), a new anti-ulcer agent, was examined. KT1-32 competitively antagonized the contraction of canine gastric arteries induced by U-46619, PGF2 alpha, and PGE2, whereas it had no effect on the PGF2 alpha-, PGE2- and LTD4-induced contraction of guinea-pig ileum, which was not affected by U-46619. In anesthetized dogs, KT1-32 significantly reduced the U-46619-induced decrease in gastric arterial blood flow. Gastric contraction induced by U-46619 in anesthetized rats was markedly inhibited by KT1-32. KT1-32 showed no influence on TXA2 synthetase and cyclooxygenase activities. These results indicate that KT1-32 is a competitive TXA2/PGH2 receptor antagonist, which may be important as to the effectiveness of KT1-32 against gastric ulcer.
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PMID:Thromboxane A2 antagonistic action of a new anti-ulcer agent, azuletil sodium (KT1-32). 259 96


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