Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric aspiration was performed continuously overnight and at hourly intervals during the daytime in 20 healthy male volunteers. Medications used included enisoprost 100, 200 or 400 micrograms, misoprostol 200 micrograms and placebo, given at bedtime. Each dose of enisoprost markedly inhibited nocturnal mean acid output, hydrogen ion activity, pH and peptic activity. The duration of these effects was up to 10 h. Misoprostol, given at bedtime, also decreased acid secretion, but the effect was significantly less than that observed with any of the doses of enisoprost. A dose-response effect for enisoprost was found for the mean nocturnal hydrogen ion activity and pH, as well as for maximum pH attained. Although enisoprost, given at bedtime, had a marked inhibitory effect on acid and pepsin secretion for the overnight interval, this did not result in rebound hyperacidity or a rise in serum total gastrin concentration. The results of this study suggest that enisoprost should be tested by clinical trial for the treatment of peptic ulcer disease.
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PMID:Twenty-four-hour intragastric measurements in twenty healthy subjects: effect of enisoprost, a novel and potent antisecretory and antipeptic synthetic E1 prostaglandin. 297 55

Serum gastrin has been reported to increase after therapy with some agents effective in the treatment of duodenal ulcer (DU). Misoprostol, a prostaglandin E1 analog, is effective in the treatment of DU, with healing rates similar to those achieved with vigorous antacid therapy or H2-receptor antagonists. Misoprostol reduces gastric acid secretion and also possesses cytoprotective properties. This multicenter study examined serum gastrin levels before and after treatment of DU patients with misoprostol. Sera for gastrin measurement were obtained from DU patients after an 8-hr fast, and 15 and 30 min after a standard mixed meal. DU patients were studied before and after two to four weeks of treatment with placebo or misoprostol: in one study, misoprostol 100 micrograms qid (without antacid) was compared with placebo; in the other study, misoprostol at 50- or 200-micrograms qid dosages (with limited antacid, Amphojel up to 54 meq/day) was compared with placebo. In addition, the serum gastrin values obtained in healthy subjects were compared with those from DU patients. Fasting and postprandial serum gastrin concentrations were essentially similar for DU patients and healthy subjects. There were no significant differences, either in fasting serum gastrin or in integrated gastrin responses, in DU patients after treatment with placebo or misoprostol at 100 micrograms (P = 0.32), 50 micrograms, or 200 micrograms doses (P = 0.85). It is concluded that misoprostol, when administered four times daily for two to four weeks at dosages required for the acceleration of DU healing, does not affect serum gastrin levels.
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PMID:Effect of misoprostol, an antiulcer prostaglandin, on serum gastrin in patients with duodenal ulcer. 308 Feb 82

Misoprostol, a synthetic prostaglandin E1 analog, has been found to be safe and effective for the treatment of peptic ulcer disease. This brief overview summarizes the gastric antisecretory effects of misoprostol in healthy human subjects using randomized, double-blind, placebo-controlled studies. Misoprostol effectively and dose-dependently inhibited basal gastric acid secretion at single doses of 50, 100 and 200 mcg/subject. Furthermore, misoprostol effectively inhibited meal-, histamine-, coffee- and tetragastrin-stimulated gastric acid secretion. The inhibition of meal-stimulated gastric acid secretion was not a consequence of the reduction of serum gastrin. In addition, misoprostol inhibited nocturnal gastric acid secretion. In these studies, the titratable acidity, volume, acid output and pepsin activity were inhibited by misoprostol. The extent of the secretory inhibition achieved with the 200 mcg dose of misoprostol was comparable to that of cimetidine administered at a 300 mg dose. The duration of the gastric antisecretory actions was in the order of 3 to 5 hours. We conclude that misoprostol is a potent inhibitor of gastric acid secretion in man.
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PMID:Perspective on the gastric antisecretory effects of misoprostol in man. 312 77

In a randomized, double-blind, crossover trial, the effects of 50-, 100-, and 200-micrograms doses of misoprostol on meal-stimulated gastric acid secretion were compared with placebo in 16 healthy male subjects. Compared with placebo, the 100- and 200-microgram doses produced significant reductions in acid output for 2 and 3 hr, respectively, following the test meal (P = 0.05). Misoprostol did not influence either the fasting or postprandial serum gastrin levels as compared with placebo. No adverse experiences were reported by any of the subjects. One subject experienced a transient rise in SGPT as compared with baseline, which may have been due to ethanol intake. This study provides a scientific rationale on which to base additional trials of misoprostol in patients with disease related to gastric acid production.
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PMID:Dose-response, meal-stimulated gastric antisecretory study of prostaglandin E1 analog, misoprostol, in man. 312 26

Misoprostol, a synthetic derivative of prostaglandin E1, was tested and shown to be an effective gastric antisecretory agent against histamine-, pentagastrin-, and meal-stimulated acid secretion in dogs. Misoprostol reduced the volume of acid secretion as well as the hydrogen ion concentration. Misoprostol did not reduce gastric mucosal blood flow, nor did it alter meal-stimulated serum gastrin levels. Misoprostol inhibited acid secretion in histamine-stimulated isolated gastric glands indicating a direct antisecretory effect on parietal cells. The potency of misoprostol was greatest when administered in direct contact with the gastric mucosa indicating local absorption and action. Misoprostol strengthened the gastric mucosal barrier as shown by the attenuation of aspirin-induced lowering of transmucosal electrical potential differences. Misoprostol protected the gastric mucosa of rats subjected to ethanol-, taurocholate-, pyloric ligation-, stress- and indomethacin-induced damage. Misoprostol also protected against indomethacin-induced intestinal lesions in rats and reduced duodenal ulcer formation in guinea-pigs and cats. The doses of misoprostol required to protect against gastric damage were about one-tenth of those required to inhibit acid secretion. The results of these and other studies indicate that misoprostol is a safe agent with unique properties that should provide a new approach for treatment of ulcer diseases of the gastrointestinal tract.
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PMID:Misoprostol preclinical pharmacology. 393 42

A model is presented that allows the assessment of acute mucosal damage in man. Damage is revealed by changes of gastric mucosal potential difference (PD), urea net fluxes and DNA shedding. Sodium taurocholate (TC) damages the mucosa in a dose-dependent fashion: 1 mM TC leads to a transient drop of PD with a subsequent rise of DNA-, but not of urea net fluxes. With 5 mM TC, the drop of PD drop lasts for more than 15 min, urea net fluxes are increased, and the rise in DNA is more pronounced. We examined in this model, whether misoprostol (SC 29333), a prostaglandin E1 derivative, could prevent the TC-induced damage. Misoprostol in an antisecretory dose lead to an overall increase of PD even in presence of TC, but did neither prevent the TC-induced drop of PD, nor the changes in urea and DNA net fluxes. Similar results were obtained, when a non-antisecretory ('cytoprotective') dose of misoprostol was given prior to TC. Misoprostol has gastrin antisecretory properties, but no cytoprotective effects against acute, taurocholate-induced mucosal damage in man.
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PMID:Bile salt-induced, acute gastric mucosal damage in man: time course and effect of misoprostol, a PGE1-analogue. 642 43