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 effects of 5-acetylspiro[benzofuran-2(3H),1'-cyclopropan]-3-one (AG 629), a newly synthesized compound, on various experimentally induced ulcers were investigated. Oral or intraduodenal administration of AG 629 in a dose range of 25-100 mg/kg inhibited water-immersion stress ulcer, exertion ulcer, Shay ulcer, indometacin- and acetylsalicylic acid (ASA)-induced gastric ulcer, and indomethacin-induced small intestinal ulcer in rats, histamine-induced gastric ulcer in guinea pigs, and ASA-induced gastric ulcer in dogs, though it was not effective against cysteamine-induced duodenal ulcer in rats. AG 629 in doses of 6.3-25 mg/kg p.o. twice a day significantly promoted the healing of acetic acid- or thermal-cortisone-induced gastric ulcers and acetic acid-induced duodenal ulcers in rats. AG 629 (25-100 mg/kg i.d.) inhibited the secretion of gastric acid and pepsin in pylorus-ligated rats and the acid secretion stimulated by distension of the rat stomach with air, whereas this compound did not affect acid secretion stimulated by histamine, pentagastrin, carbachol or 2-deoxy-D-glucose. This study shows that AG 629 has both prophylactic and curative effects on various ulcers. The anti-ulcer effect of this agent seems to be mediated primarily by increasing mucosal resistance and secondarily by an antisecretory activity.
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PMID:Effects of 5-acetylspiro[benzofuran-2(3H),1'-cyclopropan]-3-one, a new anti-ulcer agent, on experimental acute and chronic ulcers. 407 15

Metiamide greatly reduced pentagastrin-stimulated and overnight secretion of acid and pepsin in 11 patients with duodenal ulcer and virtually abolished gastric secretion in three patients with gastric ulcer. The drug was equally effective when infused intravenously or intraduodenally. A therapeutic trial of Metiamide is warranted in diseases caused or aggravated by excess gastric secretion of acid and pepsin.
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PMID:Gastric response to metiamide. 459 22

1. Experiments were designed to evaluate the effect of the pharmacological activation of beta-adrenoceptors on various models of gastric ulcer in the rat. 2. Pretreatment with the beta-adrenoceptor stimulant drugs, isoprenaline or salbutamol, significantly inhibited stress-induced gastric ulcers. This anti-ulcer effect was abolished by propranolol but not by atenolol, suggesting that beta 2-adrenoceptors mediate this response. 3. In the pylorus-ligation model, salbutamol inhibited lesion formation and reduced the intragastric content of hydrogen ions, histamine and pepsin although the latter was only affected with the higher dose of salbutamol. 4. Salbutamol also prevented the ulcerogenic action on the gastric mucosa of an exogenously perfused artificial gastric juice, showing that the anti-ulcer effect is not necessarily dependent on acid inhibition. 5. Salbutamol also reduced the formation of acute ulcers induced by various iatrogenic means (histamine, polymyxin B, reserpine and indomethacin). 6. Long-term treatment with salbutamol accelerated the healing of experimental chronic gastric ulcer. 7. In anaesthetized rats, salbutamol produced a dose-related increase in mucosal blood flow which may contribute to its mode of action. 8. It is concluded that beta-adrenoceptor agonists exert preventive and curative effects on gastric damage induced in the rat. This effect seems specific and mediated through beta-adrenoceptor activation.
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PMID:Effects of beta-adrenoceptor drug stimulation on various models of gastric ulcer in rats. 612 25

A new H2-blocker, 3-[[[2-[(diaminoethylene)amino]-4-thiazolyl]ethyl]thio]-N2-sulfamoyl propionamidine (YM 11170) inhibited gastric secretion of both acid and pepsin, when given intraduodenally to pylorus-ligated rats. The effectiveness of YM-11170 in the inhibition of acid output was 50 times as potent as that of cimetidine. The higher antisecretory activity of YM-11170 than that of 1-cyano-2-methyl-3-[2-[[(5-methylimidazol-4-yl)-methyl]thio]ethyl]guanidine (cimetidine) was also demonstrated by oral or i.v. administration. The development of gastric ulcer induced by either indometacin or acetylsalicylic acid in rats was markedly suppressed by YM-11170 with higher potency than by cimetidine. In castrated and androgenized rats, the decrease in the seminal vesicle and ventral prostate weights was not observed after treatment with YM-11170. These results suggest that YM-11170 is a potent antisecretory agent without antiandrogenic activity.
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PMID:Effect of a new potent H2-blocker, 3-[[[2-(diaminomethylene)amino]-4-thiazolyl]methyl]thio]-N2-sulfamoyl propionamidine (YM-11170), on gastric secretion, ulcer formation and weight of male accessory sex organs in rats. 612 86

Hanisch E, Schwille PO. Effects of various vagotomies and sympathectomies on gastric secretory function in the non-stressed and by immobilization stressed rat. Scand J Gastroenterol 1984, 19, Suppl 89, 99-104 The aim of the present study was to study several gastrointestinal parameters (acid, pepsin secretion, ulcer index, gastrin, somatostatin, glucagon) following various forms of sympathectomies in comparison with vagotomies under two different states of sympatho-adrenal activation in male gastric fistula rats. It is concluded that acid and pepsin appear regulated by the autonomous nervous system, even in the basal state. Gastric ulcer formation/prevention depends on gastric sympathetic innervation and on the state of activation of the adrenal medulla. Basal gastrin, somatostatin, glucagon may be modified by both limbs of the autonomous nervous system.
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PMID:Effects of various vagotomies and sympathectomies on gastric secretory functions in the non-stressed and by immobilization stressed rat. 614 96

Sucralfate is a basic aluminium salt of sulphated sucrose which is advocated for use in peptic ulcer disease. It is minimally absorbed after oral administration and is believed to act primarily at the ulcer site by protecting the ulcer from the effects of pepsin, acid and possibly bile salts. Controlled therapeutic trials have demonstrated that sucralfate 1g 4 times daily is effective in increasing the rate of healing of duodenal and gastric ulcer over a period of 4 to 8 weeks. Trials comparing sucralfate and cimetidine have not found any significant difference in efficacy between the drugs in small numbers of patients. A dosage of 2g daily given prophylactically decreases the rate of recurrence of duodenal ulcers, but the efficacy of sucralfate in preventing relapse of gastric ulcers has yet to be clearly demonstrated. Sucralfate is particularly well tolerated. Constipation, the most common side effect, occurs in 2% of patients. Thus, sucralfate offers an effective and well tolerated alternative for the management of peptic ulcer disease.
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PMID:Sucralfate. A review of its pharmacodynamic properties and therapeutic use in peptic ulcer disease. 636 84

The treatment of peptic ulcer disease has been revolutionized for both the physician and the surgeon by the development of the histamine H2-antagonists, which have become the 'gold standard' for peptic ulcer therapy. However, it has been shown that several other drugs, including antacids, can match the ulcer-healing rate obtained with histamine H2-antagonist therapy with both a high- and a low-dose regimen. An important and well-documented option is the treatment of peptic ulcer disease with sucralfate. This drug, a basic amino salt of sucrose octosulphate , acts by binding to the protein of the matrix of the ulcer crater, thus coating the ulcer against the aggressive principle of acid-pepsin and probably also by a cytoprotective effect. Sucralfate is only absorbed in minimal quantities and no metabolic interaction with other drugs is therefore likely to occur. In many studies performed on different continents it has been demonstrated that sucralfate is superior to placebo in short-term duodenal and gastric ulcer healing and that the rate of healing is similar to that obtained by cimetidine. Evidence is also accumulating that sucralfate has a place in maintenance therapy to prevent recurrence of duodenal ulcer; preliminary studies also point to benefit in the therapy of reflux oesophagitis.
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PMID:The other option in peptic ulcer therapy. 637 32

Serum group I pepsinogen (PG I) levels were measured by radioimmunoassay in patients with peptic ulcer and normal subjects. The mean (+/-S.E.) serum PG I level in 318 normal subjects was 79 +/- 3 ng/ml. The level in males, 87 +/- 2 ng/ml (n = 246), was significantly higher than in females, 72 +/- 4 ng/ml (n = 72). The serum PG I levels in the patients with gastric ulcer and in those with duodenal ulcer were 91 +/- 7 ng/ml (n = 31) and 117 +/- 10 ng/ml (n = 31), respectively. Both values were significantly higher than the value in the subjects with endoscopically normal mucosa (63 +/- 5 ng/ml). No significant change in serum PG I was observed after subcutaneous injection of tetragastrin or after ingestion of meal. A significant correlation was found between serum PG I and stimulated pepsin output, peak pepsin output, and maximal acid output and peak acid output. These findings suggest that serum PG I may be determined by the chief cell mass.
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PMID:Serum group I pepsinogen levels in patients with peptic ulcer and normal subjects. 640 6

In an attempt to determine the most appropriate procedure for surgical treatment of concomitant ulcers, gastric secretion and pathological findings were studied. Acid and pepsin secretion in concomitant gastric and duodenal ulcers was significantly higher than in case of gastric ulcer alone, and similar to the secretion seen with duodenal ulcer. Thus, vagotomy was considered an appropriate procedure. In terms of the depth, histologic activity and exposure of large blood vessels at the base of the ulcers, concomitant gastric ulcer involved serious lesions compared with concomitant duodenal ulcer, indicating that distal gastrectomy was required. Therefore, we recommend vagotomy and hemigastrectomy for concomitant ulcers, in order to preserve the physiological function of the stomach, as much as possible.
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PMID:Selection of operation for concomitant gastric and duodenal ulcers. 641 55

The sensitivity to stimuli of gastric acid and pepsin secretion in duodenal and gastric ulcer was studied using a pentagastrin dose response that was analyzed by an exponential model. By this model, maximum secretory rate (Vmax), the dose of administered pentagastrin giving 50% of Vmax (D50), and the threshold equivalent dose responsible for basal secretory rate are calculated. Using only individual tests in which the data adequately fitted the model, we report on 171 subjects, 120 with duodenal ulcer, 22 with gastric ulcer, and 29 controls. Among the possible influences on secretion, sex and weight were significant, whereas age and activity or duration of ulcer disease were not. Men secreted more acid per kilogram body weight than women in each group, and men with duodenal ulcer secreted more acid and pepsin than normal men or those with gastric ulcer. Because basal secretion in men with duodenal ulcer was a higher proportion of maximum, D50 (the measure of apparent sensitivity) was 25% lower (p less than 0.01) in patients with duodenal ulcer than in controls; when examined by sex, men with duodenal ulcer had a lower D50 than women with duodenal ulcer, men with gastric ulcer, and male controls. D50 in all patients was very much lower for pepsin than for acid. Km, the dose that would be required to stimulate secretion to 50% of maximum if basal = 0 (intrinsic sensitivity), was not different between groups or sexes. Thus the difference in sensitivity between duodenal ulcer patients and controls was seen only in the apparent, and not in the intrinsic sensitivity indices; this was largely a phenomenon of males and could be explained by a higher ratio of basal to maximal secretion. Neither the observed increase of basal nor the maximal rates of acid and pepsin secretion in duodenal ulcer patients could be explained by an increased sensitivity to gastrin.
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PMID:Apparent and intrinsic sensitivity to pentagastrin of acid and pepsin secretion in peptic ulcer. 642 36


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