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)

Adrenaline-induced gastric ulceration was studied in rats. Adrenaline in high doses caused gastric ulcer, which was completely blocked by pretreatment with alpha-blockers (phenoxybenzamine, dibenamine), but not by pretreatment with propranolol or atropine, nor by vagotomy, hypophysectomy or adrenalectomy. After successive administration of adrenaline, once daily for 7 days, however, no gastric ulcer was observed. Recovery from the ulcerogenic action of adrenaline was seen after 4 weeks withdrawal. Pretreatment with a small dose of adrenaline inhibited the ulcerogenic action of a high dose of adrenaline. Pretreatment with reserpine, pyrogallol or iproniazid inhibited the action of adrenaline. It is concluded that adrenaline has a biphasic effect on gastric ulceration, the ulcerogenic action is due to its alpha-action and antiulcerogenic effect is due to development of tachyphylaxis.
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PMID:[Biphasic (ulcer-forming and ulcer-preventing) effect of adrenaline in rats]. 0 Feb 78

Gastric juice from 15 normals, 20 patients with gastric ulcer and 14 patients with erosive haemorrhagic gastroduodenitis was investigated in respect of its activity on unheated and heated fibrin plates and its content of FDP and plasminogen or plasmin with immunochemical methods. Gastric juice from normals showed no activity on unheated and heated fibrin plates, and no FDP or plasminogen could be demonstrated. In the patients with gastric ulcer the gastric juice showed little or no fibrinolytic activity on fibrin plates except in 2, who had regurgitation of duodenal juice and neutral pH of the juice. These patients had equally high activity on heated as on unheated plates and no plasmin could be demonstrated. It was shown that this activity was not due to fibrinolysis, but to non-specific proteolytic activity (probably trypsin). The patients with erosive haemorrhage gastroduodenitis exhibited quite a different picture. The gastric juice from these patients showed extremely high activity on fibrin plates, the activity was higher on unheated than on heated plates. The activity was inhibited in vitro by addition of EACA and in vivo after administration of AMCA. The occurence of plasmic could be demonstrated directly immunologically in the gastric juice. By comparsion of plasmin and trypsin in various assays it could further be improved that the gastric juice in these cases contained plasminogen activator and plasmin. The patients with erosive haemorrhagic gastroduodenitis showed no increase in fibrinolysis in the blood, but low values for plasminogen and alpha2-M, and the serum contained FDP. These findings in the blood and gastric juice were interpreted as signs of local fibrinolysis in the stomach and duodenum. There is reason to assume that this gastric fibrinolysis contributes substantially to the bleeding tendency. The effect of administration of AMCA on fibrinolytic activity and the haemorrhage lends support to the assumption of such a mechanism.
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PMID:Gastric fibrinolysis. 0 Aug 7

Lysolecithin was isolated and identified from the gastric contents of 5 patients with gastric ulcer and erosive and atrophic gastritis. The methods used involved methanolic extration, column chromatography on silica gel and sephadex gel filtration, followed by preparative thin layer chromatography. Identification of lysolecithin was verified in one sample by thin layer chromatography and elementary analysis. A method for quantitation of lysolecithin in human gastric fluid for routine clinical analysis is described, based on the procedure used for identification of this phospholipid. Further, a hemolysis test is proposed for screening gastric contents for lysolecithin concentrations above approximately 10 mg/100 ml. With the quantitative method, an average concentration of 66.1 mg of lysolecithin in 100 ml gastric content was found in the group of 5 patients. The screening test was positive in all 5 samples, but was negative with native gastric juice in 25 persons serving as controls. When the gastric fluid of the controls was concentrated, however, 9 samples gave a positive hemolytic reaction. From these 9 specimens, the lysolecithin concentration was found to average 0.9 mg/100 ml. These findings afford evidence that lysolecithin may be involved as a factor in the pathogenesis of gastric ulceration.
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PMID:[Isolation, identification and quantitative determination of lysolecithin in the human gastric juice]. 0 72

Samples of gastric juice were aspirated every 15 minutes from 54 normal subjects and 31 patients with chronic gastric ulcers during a maximal histamine infusion test. The known tendency of patients with gastric ulcers to secrete a less acid gastric juice than that of normal subjects was confirmed. However, the hypo-acidity was related to the extent by which the total ionic concentration was less than the isotonic value of 328 mEq/l. On the assumption that such hypo-acidity was produced by the neutralisation of hydrogen ions by bicarbonate ions refluxing into the stomach from the duodenum, the data were corrected and resulted in a normal estimate of the hydrogen ion concentration in the gastric ulcer group. Independent corrections, according to the sodium content of refluxed duodenal juice, yielded similar results for the volume of gastric juice aspirated. It is concluded that while back-diffusion can explain the hypo-acidity of gastric juice in patients with gastric ulcers, duodenal reflux can explain both the hypo-acidity and the hypotonicity, and is therefore more likely to be the correct explanation.
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PMID:Hypo-acidity of gastric juice in chronic gastric ulceration caused by neutralisation. 0 97

CD-3400 developed by Nippon Chemiphar Co. Ltd., is a new antihypertensive agent belonging to the class of rauwolfa alkaloids. Influence of the agent on gastric mucosa, healing process of acetic acid-induced gastric ulcer and gastric juice in rats was investigated and compared with effects of reserpine and rescinnamine. CD-3400-induced gastric lesions were fewer in number than those produced with reserpine and rescinnamine in fasted rats. After a three day treatment of CD-3400 to fed rats, however, there were few gastric lesions, while reserpine- and rescinnamine-induced gastric lesions were aggravated to a greater extent that when a single administration was given to fasted rats. Influence of CD-3400, reserpine and rescinnamine on the healing process of acetic acid-induced ulcer was insignificant, but treatment with high doses of reserpine and rescinnamine resulted in death. Pretreatment with CD-3400 and reserpine produced a decrease in gastric acid and K+, and an increase in Na+. Repeated administration of reserpine for 5 days resulted in a decrease of both gastric volume and acid, while such was not seen with CD-3400. Treatment with anticholinergic agents such as atropine sulfate and atropine methylbromide inhibited CD-3400- and reserpine-induced gastric lesions. From these results, it would appear that cholinergic factors play a role in the pathogenesis of CD-3400-induced gastric lesions, as in the case with reserpine, and that the responses of these lesions to reserpine and CD-3400 correlate with changes of ionic fluxes in gastric juice.
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PMID:[Findings in the gastric mucosa and gastric secretion in rats treated with methyl O-(4-hydroxy-3-methoxycinnamoyl)reserpate (CD-3400) and reserpine derivatives]. 1 71

Measurements of mucosal pH of resected stomachs were carried out in gastric and duodenal ulcer patients. Low mucosal pH along the lesser curvature and relatively higher gastric pepsin levels were found. It is suggested that this lower pH affects gastric ulcer occurrence in the limited "lesser curvature area" where 63 per cent of the ulcers were situated. It is also suggested that increased pepsin activity present in gastric ulcer patients may be another factor affecting gastric ulcer formation by virtue of pepsins activated at higher pH. In duodenal ulcer patients, these factors are "overshadowed" by high acid-pepsin secretory activity of gastric juice.
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PMID:Relationship between gastric mucosal pH and site of peptic ulceration. 1 4

In 10 peptic ulcer patients, 5 duodenal ulcer and 5 gastric ulcer patients, the relation of nocturnal intragastric pH to EEG sleep stages was examined. The nocturnal intragastric pH was monitored by pH-measuring telemeter and sleep stages were recorded simultaneously by electroencephalography throughout the night. The EEG sleep stages were classified after the criteria of Dement and Kleitman. The average of intragastric pH level at each sleep stage was higher in gastric ulcer than the duodenal ulcer. The intragastric pH level became low as the patients' sleep advanced to deep stage. This tendency was more likely in duodenal ulcer patients than the gastric ulcer patients, which indicated that the cephalic phase might play an important role in the pathogenesis of hyperacidity in duodenal ulcer.
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PMID:The nocturnal intragastric pH in EEG sleep stages in peptic ulcer patients. 1 3

The enzyme, aspirin esterase, which converts acetylsalicyclic acid to the less toxic salicyclic acid, was found to be present in gastric mucosal specimens obtained from surgically resected tissue. The enzyme was found to be stable to storage and active at two pH optima. Alcohol in the reaction mixture produced a net effect of slowing the rate of aspirin hydrolysis; this was attributable to a marked inhibitory effect on aspirin esterase activity which was not completely counteracted by the increased rate of spontaneous breakdown of aspirin by alcohol. Age, sex, or gastric disease state of the patient from whom the tissue was obtained, did not significantly alter the level of enzyme activity measured, nor were different levels obtained from body or antral mucosa. In patients with gastric ulcer, those with a previous history of regular aspirin consumption did not show significantly different levels from those without such a history. It is concluded that aspirin esterase activity of gastric mucosa is not alone a significant factor in any role acetylsalicyclic acid may play in the etiology and natural history of chronic peptic ulcer.
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PMID:Aspirin esterase of gastric mucosal origin. 1 7

Eight patients with a clinical, radiology and endoscopic diagnosis of benign peptic ulcer were studied in a prospective fashion using Cimetidine (H2-Receptor antagonist). With this outgoing form of therapy the need for antiacid diminished greatly and pain totally disappeared. We discuss the possible etiological pathways of gastric ulcer and finally propose the simultaneous use of H2-Receptor antagonist and colesteramine with the goal of eliminating the two predominant factors that cause the lesion.
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PMID:[Histamine 2 receptor antagonists in the treatment of gastric ulcer]. 1 9

Conservative management of peptic ulcer relies on the use of drugs as an adjuvant to the time-honored measures of avoiding stress, reducing gastric secretion, and regulating the diet. Alkalies neutralize acid and anticholinergic drugs partly inhibit secretion.. Both are widely used but are often inadequate to control symptoms. Carbenoxolone appears to have a more specific effect in promoting healing of gastric ulcers and has now been used for 15 years. Its role in the treatment of gastric ulcer can be critrically examined, particularly in relation to how this influences surgical management. Recently introduced compounds know as histamine H2-receptor antagonists have a profound effect in inhibiting gastric secretion. Early experience in patients with duodenal ulcer indicated the efficacy of these compounds in promoting healing. These potent new drugs are likely to influence strongly the management of patients with duodenal ulcer, and this may affect the indications for surgery.
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PMID:Drugs for peptic ulcer. 1 29


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