Biomedical subjects
Publications and source records attributed to S Chono.
Explore the source record for details and available documents.
The level of endogenous prostacyclin (PGI2), prostaglandin E2 (PGE2) and thromboxane A2 (TXA2) in rat gastric mucosa was determined by radioimmunoassay to examine whether gefarnate, an antiulcer agent, maintained the endogenous prostaglandin (PG) level in rats subjected to water-immersion stress. Seven-hr immersion induced gastric lesions and a marked reduction in PGI2 and PGE2. When gefarnate was injected subcutaneously before stress exposure, the mean ulcer index was reduced and the PGI2 and PGE2 levels were maintained. Our results suggest that the reduction of endogenous PGI2 and PGE2 is a major factor in water-immersion-induced ulcers in rats, and that gefarnate inhibits this ulcer formation by inhibiting a reduction in those PGs induced by water-immersion stress.
The effects of cimetidine and gefarnate on endogenous prostacyclin, prostaglandin E2 and thromboxane were studied in vivo in rat gastric mucosa. The animals received cimetidine (20 mg/kg, i.p.) and/or gefarnate (100 mg/kg, s.c.) twice a day for 7 days. Gastric mucosal 6-keto-prostaglandin F1 alpha (as prostacyclin), prostaglandin E2 and thromboxane B2 (as thromboxane A2) were determined by radioimmunoassay. Cimetidine reduced prostacyclin, prostaglandin E2, but not thromboxane A2. Gefarnate inhibited the cimetidine-induced reduction of prostacyclin and prostaglandin E2; in cimetidine-untreated controls, it did not produce an increase in those prostaglandins and thromboxane A2 above the normal levels.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
To assess how endogenous prostaglandin (PG) in gastric mucosa acts against ulcer formation, we determined the mucosal prostacyclin (PGI2), PGE2, PGF2 alpha, and thromboxane A2(TXA2) concentrations before and after polypectomy in 6 patients in whom gastric ulcers were produced by electric burning resection of gastric polyps. These artificially induced ulcers all healed within short periods (25.7 +/- 7.4 days, mean +/- SE). Of the PGs assayed, the level of PGI2 was highest. The pG levels were increased at 4 and 7 days post-polypectomy; the most remarkable increase took place in the mucosa along the ulcer margin rather than the mucosa far from the ulcer site. We suggest that the observed increase in endogenous PGs represents a physiological response against polypectomy-induced ulcer formation.
Using radioimmunoassay, we determined the mucosal prostaglandin E2 (PGE2) concentration in normal subjects and in patients with tractable and intractable gastric ulcers. The fundic and antral mucosa of the normal subjects contained large amounts of PGE2; they were not significantly different from those found in tractable and intractable gastric ulcer patients. The mucosal PGE2 concentration at the ulcer margin was significantly higher in tractable than intractable cases. To assess the effect of PGE2 on ulcer healing, 11 intractable ulcer patients received PGE2 (1.5 or 3.0 mg/day) perorally. In 7 (64%), the ulcer healed completely within 4 to 14 weeks.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We investigated the effect of indomethacin and aspirin on the prostaglandin E2 (PGE2) levels in rat gastric mucosa. In untreated controls, the PGE2 level was 1085 +/- 80 ng/g in the fundic- and 2435 +/- 339 ng/g in the antral mucosa; it was markedly reduced by indomethacin (6 or 20 mg/kg) in a dose-related manner prior to the formation of gastric ulcers. Aspirin (200 mg/kg) also decreased the mucosal PGE2 content. The simultaneous infusion of 5 microgram/kg 16, 16-dimethyl PGE2 and 20 mg/kg indomethacin inhibited the formation of gastric ulcers. Our experimental results suggested that the indomethacin- or aspirin-induced gastric mucosal lesions are due to a deficiency of endogenous mucosal PGE2.
We investigated the effect of stress on the prostaglandin E2 levels in rat gastric mucosa. In untreated controls, prostaglandin E2 levels were higher in the antral than the fundic mucosa. Stress experiments showed tht 30-min stress induced no gastric lesions but effected a significant (p less than 0.05) increase in antral prostaglandin E2: after 7-hr stress exposure, hemorrhagic lesions and prostaglandin E2 levels significantly (p less than 0.05) below normal control values were noted. The formation of HCl-induced gastric mucosal lesions was markedly inhibited if 30-min stress preceded HCl-administration. The infusion of 5 microgram/kg 16, 16-dimethyl prostaglandin E2 prior to 7-hr stress exposure inhibited ulcer formation markedly. Our results suggested that stress-induced decrease in intramucosal prostaglandin E2 plays an important role in the pathogenesis of stress ulcer formation.
Prostaglandins protect the gastrointestinal mucosa against various ulcerogens. There are only a few reports about endogenous prostaglandins in the gastric mucosa. We present a method for determining mucosal prostaglandins and an investigation on the effect of indomethacin on prostaglandin E2 levels in the rat gastric mucosa. The levels of prostaglandins B, E1, E2, and F were higher in the antral mucosa (311 +/- 123, 632 +/- 147, 2099 +/- 455, and 415 +/- 115 ng/g, respectively) than in the fundic mucosa (33 +/- 2, 202 +/- 38, 914 +/- 229 and 138 +/- 22 ng/g, respectively). In both mucosal tissues, the prostaglandin E2 level was the highest and it was markedly reduced with indomethacin in a dose-related manner. The difference in the mucosal levels of prostaglandins suggests that in rats, mucosal damage occurs mainly in the fundus. The observed marked reduction of mucosal prostaglandin E2 following the administration of indomethacin may aid in elucidating the pathogenesis of gastric mucosal lesions induced by these types of agents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Gastric lesions were produced in rats by the administration for 2 weeks of 300 mg/kg/day of mepirizole, a basic non-steroidal antiinflammatory compound. Although the single administration of 200 mg/kg of mepirizole had no effect, the addition of water-immersion stress for one hour induced lesions not only in the corpus but also in the pyloric antrum. The administration of 250 mg/kg of mefenamic acid, an acidic non-steroidal antiinflammatory compound (insufficient for producing gastric lesions at this dose alone) with the addition of one hour of water-immersion stress induced gastric lesions. The addition of 200 mg/kg of mepirizole reduced the ulcer index from 8.1 to 4.7 in the corpus and from 4 to 0.5 in the pyloric antrum. It is suggested that basic antiinflammatory compounds inhibit gastric lesions induced by combination of acidic antiinflammatory compounds and water-immersion stress.