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)

3-hydroxy-lup-20(29) en-23-28-dioic acid (HLEDA) at doses of 50-100 mg/kg was found to be an effective anti-ulcer agent in three rat experimental gastric ulcer models: the indomethacin-induced, pyloric ligation-induced, and absolute alcohol-induced ulcers. Its anti-ulcer activities were similar to those of carbenoxolone. HLEDA was shown to increase the hexosamine levels in gastric juice collected from pylorus ligated stomachs. No influence on gastric secretion and peptic activity was observed. Carbenoxolone was found to significantly inhibit the elimination of Na+ and K+ in rat urine. HLEDA had no effect on the elimination of Na+ and K+.
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PMID:[Effect of 3-hydroxy-lup-20(29)en-23-28-dioic acid on rat experimental gastric ulcers]. 215 Mar 56

Lysolecithin has been implicated in the pathogenesis of gastric ulcer and reflux gastritis. By use of canine Heidenhain pouches, we examined effects of lysolecithin on the gastric mucosal barrier both at neutral (PO4 buffer, pH 7) and acidic (0.15 M HCl) pH with respect to interaction of lysolecithin with membrane lipids. At both pH values, 2 mM lysolecithin significantly increased forward diffusion of Na+ and backdiffusion of H+. Both solutions also caused significant efflux of membrane phospholipid and cholesterol. Saturation of neutral and acidic lysolecithin solutions with either lecithin or cholesterol significantly diminished or completely prevented disruption of the barrier to H+ backdiffusion and Na+ forward diffusion. In agreement with other reports, we also demonstrated formation of soluble lysolecithin-lecithin mixed micelles but formation of insoluble lysolecithin-cholesterol complexes. Finally, by use of [3H]polyethylene glycol and [14C]lysolecithin, we demonstrated more rapid mucosal uptake of lysolecithin at acidic than at neutral pH for any given experimental condition. Specifically, mean mucosal uptake of lysolecithin from acidic solutions saturated with lecithin (which did not disrupt the gastric mucosal barrier) was greater than uptake from neutral solutions without added lipid (which did disrupt the barrier). These studies suggest that lysolecithin-lipid interactions play an important role in lysolecithin-induced injury to the gastric mucosa. The most important of these interactions appears to occur in luminal lysolecithin micelles rather than within mucosal membranes.
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PMID:Lysolecithin-lipid interactions in disruption of the canine gastric mucosal barrier. 242 Feb 4

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

Glycyrrhetinic acid (Ia) and eighteen related derivatives were examined for antiulcer activity using stress-induced gastric lesions (restraint plus water immersion at 25 degrees C) in mice and rats as screening tests. Among the compounds tested, dihemiphthalate derivatives of 18 alpha- or 18 beta-olean-12-ene-3 beta,30-diol (IV, IIId), 18 beta-olean-9(11)12-diene-3 beta,30-diol (VIc), and olean-11,13(18)-diene-3 beta,30-diol (VIIc) showed potent inhibition of gastric lesion formation at a dose of 12 or 25 mg/kg (p.o.); carbenoxolone sodium (Ib) significantly suppressed the lesion formation at a dose of 500 mg/kg (p.o.). Further evaluation of the antiulcer activity was carried out mainly for compound IIId. Compound IIId (p.o.) prevented the formation of indomethacin-induced or 0.6 N HCl-induced gastric lesions; the latter antiulcer effect was noted even in the combined treatment with indomethacin, suggesting that the effect occurs independently of endogenous prostaglandins. In contrast, compound IIId had no preventive effect against Shay rat ulcer when intragastrically (i.g.) administered; further, no antisecretory effect was seen by i.g. application in pylorus-ligated rats. Administration of compound IIId for 2 weeks accelerated the healing rate of acetic acid-induced gastric ulcer in rats. No significant change in urine excretion was observed after its consecutive administration for 3 d. These results suggest that dihemiphthalate derivatives (IIId, IV, VIc, VIIc) may produce a strong antiulcer activity, probably by strengthening some gastric mucosal defensive mechanism.
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PMID:Antiulcer activities of glycyrrhetinic acid derivatives in experimental gastric lesion models. 260

A review of the literature indicates that sucralfate attains a healing rate of 79 percent for duodenal ulcer and 75 percent for gastric ulcer in four and eight weeks, respectively, rates not different from those reported for cimetidine and ranitidine. Meta-analyses show that, whereas cigarette smoking significantly affects duodenal ulcer healing by acid-reducing agents, the healing rates of smokers and non-smokers treated with sucralfate are indistinguishable, suggesting an inherent advantage through the underlying mechanisms of the drug. Pooling reports in the literature indicates that the 12-month relapse curves of duodenal ulcers initially healed with sucralfate and colloidal bismuth subcitrate closely overlap each other and are significantly lower than the curves of the histamine (H2)-receptor antagonists under comparison. A review of the ulcer relapse rates following initial healing in the literature shows that patients receiving acid-reducing agents such as antacids, H2-receptor antagonists, and omeprazole have relapses at similar rates. Use of anticholinergics or non-antisecretory agents including carbenoxolone sodium is associated with a longer remission. Preliminary evidence is available to support the concept that the use of acid-reducing agents results in up-regulation, whereas the use of anticholinergics and non-antisecretory agents is associated with down-regulation of the parietal cells. These changes at the molecular level may help to explain the differences in relapse rates following initial healing with various anti-ulcer agents.
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PMID:Implications of sucralfate-induced ulcer healing and relapse. 266 May 54

Two cases of miliary tuberculosis with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) were reported. Case 1. A 70-year-old woman suffering from general fatigue and appetite loss developed neck stiffness and stupor three days after admission. The chest X-ray film showed a miliary pattern in both lungs. The lumber puncture showed high pressure and increased leucocytes in the cerebrospinal fluid. Serum natrium concentration was 113 mEq/L. Tubercle bacilli were seen in the broncho-alveolar lavage fluid by the Ziehl-Nielsen staining. An improvement in electrolytes balance was produced by 2.5% NaCl and antituberculous treatment, then her mental function recovered. Case 2. A 71-year-old man was admitted with gastric ulcer. When he developed dry cough thirty days after admission, the chest X-ray film showed a miliary pattern in both lungs. Acute respiratory failure advanced concomitantly. Tubercle bacilli were seen in the sputum (Gaffky 5) by the Ziehl-Nielsen staining. Antituberculous treatment was started. Although the miliary shadow improved gradually, hyponatremia was rather progressing. The following values for serum constituents were determined: sodium, 118 mEq/L; antidiuretic hormone, 10.3 pg/ml. Antituberculous treatment and supplement of NaCl (10 g/day) improved serum natrium level. He had no mental disturbance in his clinical course. In both cases, thyroid, renal and adrenal function were normal. Systemic edema and dehydration did not exist at the state of hyponatremia, and it was very clear that laboratory data were compatible with SIADH criteria. Miliary tuberculosis is one of the least commonly recognized causes of SIADH.
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PMID:[Two cases of miliary tuberculosis with SIADH]. 279 13

The aetiology of ethanol-induced gastric ulceration, and its interaction with zinc, were studied in rats. Oral administration of ethanol (40, 50 or 80%) to conscious rats reduced the stomach mucus content and increased gastric ulcer formation in a concentration-dependent manner. Histological examination indicated that mucus, both on the surface and within the epithelium, was depleted because of epithelium being shed from the gastric mucosa. Zinc sulphate abolished mucus loss and ulcer formation in the ethanol-treated animals. Using an ex-vivo gastric chamber preparation in anaesthetised animals, it was found that an ethanol (50%)-HCl (100 mmol/l) solution produced severe glandular haemorrhagic ulceration, elevated Na+, K+ and protein levels in the luminal solution, and reduced the H+ content in this fluid. Zinc sulphate pretreatment dose-dependently prevented all these changes. On the other hand, prostaglandin E2 (PGE2) administration only antagonised ethanol ulceration and H+ loss from the chamber; it did not significantly influence the Na+ and K+ fluxes and protein leakage into the luminal solution. It is concluded that the antiulcer mechanisms of zinc sulphate and PGE2 may be different. Protection by the former drug could be due partly to preservation of mucus adhering to the gastric mucosa. The possibility of the membrane-stabilising action of zinc contributing to the observed effects is also discussed.
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PMID:Protection by zinc sulphate against ethanol-induced ulceration: preservation of the gastric mucosal barrier. 294 51

Seventy-two perforated gastroduodenal ulcers were treated by an original method aimed at avoiding emergency surgery, which consists of peritoneal dialysis associated, during 3 days, with gastric aspiration. Over a 3-year period this method was applied to all patients admitted with a perforated ulcer. The ulcer was revealed by the perforation in 25 p. 100 of the cases, and 90 p. 100 of the patients had pneumoperitoneum. Contrast radiography with Gastrografine (sodium and meglumine amidotrizoate) located the perforation. Fifteen patients had another disease which made the prognosis worse. The time elapsed between perforation and treatment was 15 hours on average. Peritoneal fluid infection was present in 30 p. 100 of the cases. The outcome was favourable in 69 patients (96 p. 100). One patient died of pulmonary embolism, another was operated upon on the 4 th post-perforation day for a bleeding ulcer and a third patient with giant gastric ulcer developed subphrenic abscess. This method seems to be indicated in patients at high surgical risk (elderly people or people with severe underlying disease), and in young patients with perforated acute ulcer. In chronic ulcers, peritoneal dialysis ties the patient over the first hours, thus enabling radical surgery to be electively performed. In perforations seen after 24 hours, it helps in supporting the patient prior to surgery. The method in contra-indicated in gastric ulcers.
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PMID:[Perforated gastroduodenal ulcers. Treatment by peritoneal dialysis. 72 cases]. 296 79

The effect of lithium preparations (lithium carbonate, lithium oxybutyrate), calcium channel blocking agents (verapamil, nifedipine), beta 2-adrenoagonist (salbutamol), cromolyn sodium and cimetidine on clinical efficacy and frequency of ulcer cicatrization was assessed in 201 patients (33 women, 168 men) with endoscopically verified stomach ulcer (52 patients) and duodenal ulcer (166 patients) during treatment for 4 weeks as compared to placebo and standard antiulcerative therapy (cholinolytics, antacids and reparents). All the tested drugs (excluding cromolyn sodium) significantly increased as compared to placebo the frequency of ulcer cicatrization (p less than 0.001 in the use of lithium preparations and cimetidine; p less than 0.01 in the use of salbutamol and verapamil; p less than 0.05 in the use of nifedipine). The effect of lithium preparations and cimetidine exceeded that of standard antiulcerative multimodality therapy.
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PMID:[Randomized double-blind placebo-controlled study of drugs with anti-ulcer action and their use in associated pathology]. 312 6

Effects of (-) cis-2,3-dihydro-3-(4-methylpiperazinylmethyl)-2-phenyl-1,5-benz othiazepin-4-(5H ) -one hydrochloride (BTM-1086) on various experimental gastric and duodenal ulcers were studied in rats. In the pylorus-ligated ulcer, restraint and water immersion stress ulcer, and drug-induced ulcer (indomethacin, aspirin, reserpine, serotonin, cysteamine), BTM-1086 prevented the development of ulcer at a dose of 0.1 to 1 mg/kg, p.o., but only weakly inhibited the histamine-induced gastric ulcer. The inhibitory activities of BTM-1086 were significantly higher than those of atropine sulfate. In the healing experiment with the acetic acid-induced stomach ulcer, BTM-1086 (1 mg/kg/day, p.o., X 14) showed a significant healing effect, which was higher than that of propantheline bromide. BTM-1086 at a dose of 0.2 mg/kg, i.d., remarkably inhibited the gastric secretion 6 hr after pylorus ligation. The aspirin-induced reductions of the total acid and K+ as well as the increments of the volume and Na+ in the gastric secretion were prevented dose-dependently by pretreatment with BTM-1086.
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PMID:Antiulcer effect of (-)-cis-2,3-dihydro-3-(4-methylpiperazinylmethyl) -2-phenyl-1,5-benzothiazepin-4-(5H)-one hydrochloride (BTM-1086) in experimental animals. 376 47


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