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)

We previously reported that cysteamine induces severe gastric ulcers in WKY, but very mild in SHR. The aim of this study is to elucidate the role on the sympathoadrenal medullary system in the pathogenesis of the cysteamine-induced gastric ulcer. Catecholamine (CA) contents in the stomach and adrenal gland were significantly higher in the non-treated SHR than in the non-treated WKY, suggesting that the sympathetic nervous system is more facilitated in SHR. Cysteamine decreased the noradrenaline and adrenaline contents in these tissues in both strains, however the values of CA was still higher in the treated SHR than the non-treated WKY. Histologically the adrenal medulla was severely damaged by cysteamine administration in WKY than in SHR. In contrast an immunohistological study revealed that chromogranin reactivity of the adrenal medulla was significantly stronger in the treated SHR than in the treated WKY. The celiac plexus was well preserved morphologically even in the cysteamine treatment in both strains. These results suggest that the capacity of the sympathetic nervous system in both the adrenal medulla and the stomach plays an important role in preventing the cysteamine-induced gastric ulcer in SHR.
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PMID:[Inhibition of the cysteamine-induced gastric ulcer by the sympathoadrenal medullary system in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY)]. 175 79

The possible role of sulfhydryls in indomethacin-induced gastric mucosal injury was studied. No significant decrease of the contents of both non-protein and protein-binding sulfhydryls was observed in the gastric mucosa during injury. Indomethacin-induced gastric ulcer was inhibited by cysteamine of 132 and 264 mumol, i.g. or of 132 mumol, s.c. by 82%, 92% and 75% respectively. Such protective effect was not observed with cysteine in equal molar dose. Subcutaneously injected cysteamine (132 mumol) inhibited gastric acid secretion by 46% in indomethacin-treated rats, while no effect was observed on acid secretion when cysteamine was given intragastrically. Cysteamine, given through both routes, did not affect gastric barrier mucus secretion. It is suggested that sulfhydryls in gastric mucosa are not involved in the mechanism of indomethacin-induced injury and that the potent cytoprotective effect of cysteamine against indomethacin-induced ulcer maybe not caused by its sulfhydryl group.
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PMID:[The role of sulfhydryls in indomethacin-induced gastric mucosal injury in rats]. 260 58

The physiological roles of sympathetic nerve system in the stomach has been thought to be very important in the pathogenesis of peptic ulceration. The aim of this study was to examine the effects of dopamine receptor agonists and antagonists on gastric acid secretion and gastroduodenal ulcer formation induced by cysteamine injection in rats. Cysteamine was given by subcutaneous injection as 400mg/kg in doses. Dopamine was given by continuous iv infusion as 2, 4 and 8 micrograms/kg/min in doses. Domperidone regarded as antagonists of D2 receptor was given by continuous iv infusion as 2 micrograms/kg/min in doses. As a result of acid output measured during infusion of dopamine alone or dopamine with domperidone in non-vagotomized or vagotomized rats, increasing effects of dopamine on acid output were depended on dopaminergic mechanism, and decreasing effects of dopamine on acid output were depended on dopaminergic mechanism in rami vagus. As a result of duodenal and gastric ulcer index, ulcerogenicity of cysteamine in the stomach was concerned with dopaminergic mechanism more than that of in the duodenum. These results suggested that the pathogenesis of experimental ulcer induced by cysteamine injection was depended on dopamine receptor in the stomach.
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PMID:[Effects of dopamine receptor agonists and antagonists on an experimental ulcer system induced by cysteamine in rats--dopaminergic mechanism vs pathogenesis of peptic ulceration]. 318 69

Cysteamine given three times within 8 h produced severe duodenal and gastric ulcers in female SIV rats. A pentobarbital anesthesia during the first 10 h prevented gastric ulcer formation without affecting duodenal ulcer. An additional 10 h lasting intragastric infusion with 0.6 ml/h Ringer containing 5 mmol/l of a mixture 3: 1 pure taurocholic and glycocholic acid or 20 and 50 mmol/l pure taurocholic acid in 0.2 N HCl did not reverse the protective effect of pentobarbital, e.g. incidence and intensity of gastric ulcer did not change. Treatment with somatostatin significantly reduced the intensity of duodenal ulcer. The inhibition of cysteamine-induced gastric ulcer formation by pentobarbital does not seem to be due to a possible inhibition of duodenogastric reflux but more likely to an inhibition of central nervous stress reactions by anesthesia.
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PMID:Effect of pentobarbital anesthesia and bile acids on cysteamine-induced duodenal and gastric ulcers in rats. 614 97