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)

Gastric ulcer development and changes in the contents of glucose, free fatty acids (FFA), and K and Ca ions in the blood were studied in rats subjected to a graded stress of immobilisation and cold. During stress the volume of secretion and the output of HCl, decreased although the concentration rose slightly. Chlorpromazine (CPZ), thioridazine (TRZ), spiroperidol (SPI), and fluphenazine (FLU) inhibited to various degrees ulcer formation during stress. SPI reduced stress-induced mucosal damages in 94%, but FLU even in doses 100 times smaller than those of the other drugs counteracted ulcer formation. CPZ, TRZ and SPI in preventive doses increased proportionally the blood glucose level both in control rats and in those subject to stress. FLU in effective doses produced no hyperglycemia either in control rats or in those exposed to stress. We conclude that the prevention of gastric ulcer development by neuroleptics may be the result of their antisecretory action and counteracting of breakdown of sympathetic activity during severe stress.
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PMID:The effect of neuroleptics on the development of gastric ulcers in rats exposed to restraint-cold stress. 126 58

A series of new N-phenylbenzamido acid derivatives was synthesized and evaluated for their ability to inhibit the IgE-mediated passive cutaneous anaphylaxis in the rat (PCA), as well as for their capacity to inhibit gastric mucosal damage induced by the oral administration of absolute alcohol in the rat. Some of these new derivatives exhibit potent antiallergic and cytoprotective activity, 20-80 times higher than that of the reference, disodium cromoglycate (DSCG). Structure-activity relationships are discussed. The antiallergic activity of one of the more potent compounds of this series, i.e. 4-(1H-tetrazol-5-yl)-N-[4-(1H-tetrazol-5-yl)phenyl]benzamide (compound 44, CR 2039) was further evaluated in vivo. This compound antagonizes the bronchoconstriction induced by aerosolized ovalbumin in both anesthetized and conscious IgE sensitized guinea pigs with ID50 of 3.7 mg/animal (tracheal insufflation) and 20 mg/kg (im). Further cytoprotective effects were evaluated in gastric ulcer models induced by the acute oral administration of hypertonic sodium chloride solution or by acetic acid and by the subchronic administration of glucose in fasted animals. In the models used experimentally CR 2039 is effective, whereas DSCG seems to be devoid of any protective activity. Such a potent antiallergic and mucosal protectant could provide a new potential agent in the therapy of atopic allergic diseases.
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PMID:Antiallergic and cytoprotective activity of new N-phenylbenzamido acid derivatives. 143 73

The effect of calcitonin on gastric emptying of a radiolabelled test meal was examined in 8 male patients with active gastric ulcer. The patients ate the test meal twice, whilst during one of the examinations they were given synthetic salmon calcitonin (415 pmol i.v. bolus + continuous infusion during 90 min to reach an overall dose of 62.25 pmol.kg-1 body mass) and during the other one they received placebo--in randomized order, according to a double-blind study protocol. In every patient a pronounced delay in gastric emptying after calcitonin was observed --the emptying index, Ix: 2.33 +/- 0.22 x 10(-2) min-1 (placebo) vs 0.81 +/- 0.18 x 10(-2) min-1 (calcitonin), p less than 0.001. Calcitonin delayed and significantly lowered the postprandial gastrin release, as well as suppressed the postprandial insulin release with a secondary change in the serum glucose concentration pattern, whereas the serum calcium and phosphorus remained unaffected. The authors conclude that salmon calcitonin in a pharmacological dose elicits a strong inhibitory effect on gastric emptying in gastric ulcer patients.
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PMID:[Effect of calcitonin on gastric emptying after isotope-labeled solid meal in patients with stomach ulcer]. 209 24

To determine its efficacy and safety in treating obesity, a silicone-rubber balloon was passed into the stomach of 10 nondieting, obese subjects. In a counterbalanced sequence, the balloon was inflated with 400 mL for 1 mo and deflated for 1 mo. Lower intakes of solid and liquid test meals (NS), significantly slower gastric emptying, and concomitant changes in glucose, insulin, glucagon, and cholecystokinin concentrations consistent with slower emptying resulted during balloon inflation. After balloon inflation, one small gastric ulcer developed, which subsequently healed. Significant weight loss occurred during the second and third week of the inflation period (F[1,9] = 5.0, p less than 0.05). However, the weight loss was small and the significant effect did not continue through the fourth week.
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PMID:Gastric balloon to treat obesity: a double-blind study in nondieting subjects. 218 57

In a double-blind placebo-controlled study, the effect of calcitonin on gastric emptying and on serum concentrations of gastrin, insulin, glucose, calcium and phosphorus after a mixed solid-liquid meal was examined in six patients with type I gastric ulcer. Synthetic salmon calcitonin 415 pmol i.v. was given as a bolus followed by a 90-min infusion to reach an overall dose of 62.25 pmol.kg-1. Gastric emptying of a radiolabelled meal was measured with a gamma camera. Calcitonin suppressed gastric emptying in all patients examined. The mean gastric transit time, MTT90, increased from 38.1 +/- 0.4 min after placebo to 43.1 +/- 0.6 min after calcitonin (P less than 0.001). Calcitonin significantly blunted the postprandial gastrin release: AUC0-90 10,398 +/- 2886 ng. l-1 min (placebo) and 8238 +/- 2573 ng. l-1 min (calcitonin), P less than 0.05, and abolished the postprandial insulin release--AUC0-90 2244 +/- 230 mU.l-1 min (placebo) vs. 638 +/- 198 mU.l-1 min (calcitonin), P less than 0.01. A steady increase in the serum glucose during calcitonin infusion, reaching up to 5.6 +/- 0.31 mmol.l-1 at the end of the infusion, was observed. Calcitonin did not significantly affect serum calcium or phosphorus concentrations. The authors conclude that a delayed gastric emptying is to be expected in patients undergoing calcitonin treatment.
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PMID:Effect of calcitonin on gastric emptying and on postprandial gastrin and insulin release in patients with type I gastric ulcer. 221 26

Low doses of insulin (less than 1.25 IU/kg body weight) stimulate gastric acid secretion in the rat, whereas higher doses (greater than 2.5 IU/kg) release gastrin and cause gastric ulcers but do not increase acid secretion. In this study we have characterized the ulcerogenic properties of insulin in the rat. A dose of 5 IU/kg subcutaneously proved to be maximally effective. Ulcer formation was rapid, and the maximum 90% incidence was reached after 5 h. Both glucose administration and food intake protected against the ulcerogenic effects of insulin. The effects of anti-ulcer drugs and of vagotomy on insulin-induced ulcers were also studied. Animals were divided into seven groups: 1) saline, 2) omeprazole, 3) ranitidine, 4) sucralfate, 5) bilateral vagotomy, 6) unilateral vagotomy, and 7) antrectomy. Medical treatment was continued for 6 days before insulin administration, operations having been performed 6-8 weeks earlier. Insulin was injected subcutaneously in a dose of 5 IU/kg. Five hours later stomachs were inspected for ulcers. Neither the antrectomized rats nor those treated with omeprazole or ranitidine had ulcers. In the saline- and the sucralfate-treated groups the gastric ulcer incidence was 83% and 80%, respectively, with a mean of six and seven ulcers per rat. Ulcers were evenly distributed between the two sides of the stomach. Rats that had undergone bilateral vagotomy (which abolishes gastric acid secretion and causes hypergastrinemia) responded to insulin with an ulcer incidence of 5%. In the unilaterally vagotomized rats there were only 2 ulcers on the denervated compared with 37 on the innervated side.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin-induced gastric ulcers in the rat. 331 Jan 98

Three patients had autopsy-proved peritoneal lymphomatosis with ascites. Ascitic fluid analysis was characteristic in that the total protein level was greater than 2.5 g/dL, the lactate dehydrogenase level was greater than 225 mU/mL (the upper limit of normal for serum), and the glucose level was less than 50 mg/dL in all patients. Atypical cells were noted on ascitic fluid cytologic studies, and peritoneoscopic biopsy specimens were diagnostic of lymphoma in all three cases. Gut ulceration was present in all patients; a gastric ulcer, a duodenal ulcer, and a colonic ulcer were found to have invasion by lymphoma at autopsy. No patient lived long enough to receive chemotherapy. Perhaps if the diagnosis of lymphoma could have been made earlier, their lives could have been prolonged.
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PMID:Peritoneal lymphomatosis with ascites. A characterization. 396 80

Fasting serum gastrin has been measured by radioimmunoassay in 72 patients with duodenal ulcer and compared with that in normals, patients with gastric ulcer, and with the Zollinger-Ellison syndrome. The mean (+/- SEM) gastrin levels were 15.7 +/- 1.5 pg/ml in the duodenal ulcer group, 32.1 +/- 4.3 pg/ml in normals, 118 +/- 18.1 pg/ml in gastric ulcer, and between 450 and 2,000 pg/ml in the Zollinger-Ellison syndrome. There were no difficulties in distinguishing simple ulcer from the Zollinger-Ellison syndrome as the presence of hyperchlorhydria in combination with hypergastrinaemia led to a confident diagnosis of the latter disease.The effect of protein, glucose, and cream feeding with and without atropine was also assessed in a group of these patients with duodenal ulcer. As in normals, there was no stimulation of gastrin release by either atropine alone, distilled water, glucose, or cream. However, protein alone produced a greater rise in serum gastrin levels compared with that in normals and prior atropinization augmented this response greatly in duodenal ulcer. This indicates an increased amount of releasable gastrin in the latter disease, the release of which, under basal conditions, is suppressed by the high acidity in the antrum.
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PMID:Serum gastrin in duodenal ulcer. I. Basal levels and effect of food and atropine. 513 20

Electrical stimulation (ES) of the nucleus amygdaloideus centralis ( NAmC ) and basolateralis ( NAmBL ), like norepinephrine, decreased mucosal blood flow of the gastric antrum and duodenum and decreased antral motility amplitude in gallamine-immobilized cats. ES of the nucleus lateralis hypothalami (NHL) less extensively produced a similar action. The NAmC stimulation elevated BP and renal sympathetic discharges, whereas the NAmBL stimulation lowered BP. These findings indicate that the gastric and pressor responses to the NAmC stimulation may be attributed to an increase in cerebral sympathetic outflow. Bromazepam dose-dependently (0.1 approximately 1.0 mg/kg, i.v.) prevented these gastric, pressor and renal sympathetic responses to the NAmC stimulation, but it did not alter the depressor response to the NAmBL stimulation or the norepinephrine-induced reactions. Bromazepam less extensively attenuated the gastric and pressor responses to the NHL stimulation. Moreover, bromazepam inhibited stress-induced gastric ulcer formation in rats more markedly than cimetidine, sulpiride and metoclopramide. Bromazepam markedly decreased stress-induced selective increase in the glucose utilization rate in the NAmC among various amygdala nuclei. These results indicate that effects of bromazepam on the gastric and pressor responses to the NAmC stimulation may be due to the inhibition of central sympathetic outflow, and the NAmC are more sensitive to bromazepam than the NHL and other amygdala nuclei.
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PMID:[Effects of bromazepam on responses of mucosal blood flow of the gastrointestinal tract and the gastric motility to stimulation of the amygdala and hypothalamus in conscious cats]. 614 17

These experiments were carried out to supplement the pharmacodynamic profile of 2[1-(2,6-dichlorophenoxy)-ethyl]-2-imidazoline hydrochloride (lofexidine, Lofetensin and Loxacor), a potent hypotensive imidazoline derivative with a central mode of action. Effects indicative of a central sedative action were seen in various experiments on mice and rats. However, comparative studies with clonidine, particularly those involving the interaction with hexobarbital, the effect on motor coordination on a rotating rod, the effect on body temperature and other experiments, indicated that lofexidine had a 10 to 100 fold less sedative effect than clonidine, depending on the test and the route of administration. In rats there was a dose-related, diuretic and saluretic effect. This effect was not seen in dogs. In rabbits and guinea pigs, lofexidine exhibited local anaesthetic effects and its potency and duration of action were comparable to those of the reference compounds (tetracaine or mepivacaine). Lofexidine did not modify gastric secretion in rats. On the other hand, it inhibited chemically induced (phenylbutazone) and stress-induced (swimming) gastric ulcer formation in rats. Antiinflammatory and analgesic activities in rats and mice were, at most, very weak. Lofexidine increased blood glucose levels of normoglycaemic rats; clonidine is known to have the same effect. In order to investigate the possibility of combining lofexidine with a diuretic drug for the treatment of hypertension, the interaction with hydrochlorothiazide was studied in some experiments. The results obtained from these experiments showed that there was no adverse effect and the diuretic and saluretic effects of hydrochlorothiazide were not impaired. No findings militated against the use of lofexidine as an antihypertensive drug. It is likely that lofexidine, in contrast to clonidine, has less marked central sedative effects.
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PMID:Animal experiments on the safety pharmacology of lofexidine. 689 Mar 67


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