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Biomedical subjects

S Okabe

Publications and source records attributed to S Okabe.

At least 487 records · Page 27Linked to original sources
PubMed1982

Electron microscopic studies on retinochoroidal atrophy in the human eye.

Nine eyeballs were enucleated from nine patients with excessive myopia, secondary retinochoroidal atrophy, absolute glaucoma, uveal malignant melanoma, Behçet's disease and sympathetic ophthalmia. The retina and choroid were studied with light and electron microscopes. The results were: In excessive myopia, marked blockade of choriocapillaries was accompanied by progressive retinal degeneration. In secondary retinochoroidal atrophy induced by retrobulbar fibrosis, the choriocapillaries were partially blocked and the retina had markedly degenerated. In Behçet's disease, exudative inflammation was recognized in the choroid extending to the retina and causing retinal detachment, though the choriocapillaries remained morphologically normal. In sympathetic ophthalmia, both the choriocapillaries and the retina remained normal, though marked inflammation was recognized in the outer layer of the choroid. In absolute glaucoma, the fine structures of the choriocapillary were well preserved in spite of bulbar hypertonia. In uveal malignant melanoma, the ultra structure of the choriocapillary near the tumor was well preserved. The choriocapillaries were normal even when the retina had degenerated. Retinal degeneration was recognized when changes such as blockage, disappearance, dilatation and increased permeability were found in the choriocapillaries. Damage to the choriocapillaries might play an important role in inducing and developing retinochoroidal atrophy.

Adult↗
PubMed1982

Effects of prolonged treatment of pirenzepine 2HCl on gastric secretion and plasma gastrin levels in rats.

Gastric secretory functions and plasma gastrin levels in rats after the prolonged treatment of pirenzepine 2HCl were evaluated. Pirenzepine 2HCl at 100 mg/kg was given p.o. twice daily for 4 weeks. Control animals were given saline alone. The test agent potently inhibited gastric secretion in pylorus-ligated rats and fistula rats stimulated with pentagastrin and histamine before and after cessation of 4 weeks' treatment. At 1 day after the treatment, the acid output slightly decreased in pylorus-ligated rats and significantly decreased in fistula rats stimulated with secretagogues. At 3 days, the acid output was slightly increased in pylorus-ligated rats and significantly increased in fistula rats stimulated with pentagastrin but was unchanged in the case of histamine stimulation. At 10 days, the gastric secretion in pylorus-ligated rats tended to increase but the acid output in fistula rats was not affected. Pirenzepine 2HCl increased the plasma gastrin levels in normal rats and at 1 day after the treatment, but had no effects at 3 and 10 days. Propantheline Br showed much the same results as seen with pirenzepine 2HCl. Cessation of prolonged treatment with pirenzepine 2HCl appears to increase only slightly and transiently the sensitivity of gastric secretory cells.

Animals↗
PubMed1981

Effects of cholestyramine and synthetic hydrotalcite on acute gastric or intestinal lesion formation in rats and dogs.

Cholestyramine, a bile-binding agent, markedly inhibited the development of gastric lesions induced by water-immersion stress in rats and of gastric and intestinal lesions induced by indomethacin in rats and dogs with an intact pylorus. However, cholestyramine had no effect on gastric lesions induced by stress in pylorus-ligated rats and on aspirin-induced gastric lesions in rats and dogs with or without pylorus ligation. Hydrotalcite, a potent antacid, significantly inhibited the gastric lesions induced by stress and aspirin in rats and dogs with or without pylorus ligation. Hydrotalcite also inhibited the gastric lesions induced by a single administration of indomethacin in rats with an intact pylorus. In contrast, the agent had no effect on gastric and intestinal lesions induced by repeated administration of indomethacin to rats and dogs with an intact pylorus. These results suggest that while bile probably plays an important role in the pathogenesis of stress-induced gastric lesions and of indomethacin-induced gastric and intestinal lesions, bile does not appear to play a role in the pathogenesis of aspirin-induced gastric lesions.

Aluminum Hydroxide↗
PubMed1981

Does indomethacin activate healed gastric ulcers in the dog?

Effects of indomethacin on healed partially healed gastric ulcers in the dog were studied. Gastric ulcers were produced by submucosal injection of 1 ml of 40% acetic acid solution into the bordering area of the fundus and antrum of the stomach. Indomethacin, 20 mg/kg, was given orally once daily for 5 days beginning on the 50th day after ulceration. While erosions or deep ulcers were produced by indomethacin, healed or partially healed acetic acid ulcers were not aggravated. Mechanisms involved in this strong resistance of healed ulcers to the ulcerogenic agent remain to be determined.

Animals↗
PubMed1981

[Effects of ranitidine, a new histamine H2-receptor antagonist, on histamine- and aspirin-induced gastric ulcers in rats and dogs (author's transl)].

Male donryu rats (200-220 g) and mongrel dogs of both sexes (7-20 kg) were used. Histamine-induced ulcers: Histamine 2HCl (100 mg/kg) was given i.p. to 24 hr-fasted rats and the animals were killed 4 hr later. Histamine 2HCl in beeswax (20 mg/kg) was given i.m. to dogs once daily for 5 days and the animals were killed on the 6th day. Aspirin-induced ulcers: Aspirin (100 mg/kg) was given p.o. to the 24 hr-fasted rats and dogs twice (15 h apart) and the animals were killed 9 hr after the second administration of aspirin. Either the length (mm) or ares (mm2) of each ulcer was measured, summed, and used as an ulcer index. Cimetidine and gefarnate were used as reference drugs. Ranitidine dose-dependently inhibited both histamine- and aspirin-induced ulcers in rats and dogs. On the basis of ED50, the antiulcer effect of ranitidine on histamine-induced ulcers was about two times (in rats) or 9 times (in dogs) more potent than cimetidine. However, the antiulcer effect of ranitidine on aspirin-induced ulcers was 1.7 times more potent than cimetidine (in rats) or almost equal (in dogs) to cimetidine. Gefarnate had an insignificant effect on both histamine- and aspirin-induced ulcers.

Animals↗
PubMed1981

Effects of N-acetyl-L-carnosine aluminum (CL-1700) on various acute gastric lesions and gastric secretion in rats.

Effects of a newly synthesized compound, N-acetyl-L-carnosine aluminum (CL-1700), on the formation of various types of acute gastric lesions were studied in rats. CL-1700 at 300 or 1,000 mg/kg (p.o.) significantly inhibited Shay ulcers and water-immersion stress- and aspirin-induced erosions in pylorus-ligated rats, and indomethacin- or phenylbutazone-induced erosions. CL-1700 had a weak effect on water-immersion stress-induced erosions in rats with an intact pylorus. CL-1700 at 100 or 300 mg/kg (i.p.) significantly inhibited Shay ulcers and water-immersion stress-induced erosions in rats with an intact pylorus. However, this compound (i.p.) had no effect on aspirin- and indomethacin-induced gastric erosions. CL-1700 at 1,000 mg/kg (i.d.) significantly reduced the gastric acid output in pylorus-ligated rats but at 300 or 1,000 mg/kg (p.o.) increased the volume, pepsin output and raised the pH value. The effects of CL-1700 on experimental gastric lesions were slightly weaker than those of aluminum sucrose sulfate but almost equal to or better than those of cimetidine. However, the effects of CL-1700 were much more potent than those of gefarnate. As CL-1700 appears to be a promising new anti-gastric lesion agent, the mechanisms of action are now under investigation.

Animals↗
PubMed1981

[Effects of a new histamine H2-receptor antagonist, ranitidine, on experimental acute gastric and duodenal ulcers (author's transl)].

Ranitidine at 100 to 200 mg/kg (i.d. or p.o.) potently inhibited the development of Shay ulcers, indomethacin- or phenylbutazone-induced gastric ulcers and histamine-carbachol-induced duodenal ulcers in rats. Ranitidine at 100 mg/kg (p.o.) also inhibited the development of water-immersion stress-induced gastric ulcers in rats, histamine-induced gastric and duodenal ulcers in guinea pigs, even though the inhibition rate remained within 70%. At that time, the gastric acid output in guinea pigs was reduced with some doses of the drug. Cimetidine at 100 to 200 mg/kg (p.o.) also inhibited the development of indomethacin-, phenylbutazone-, and water-immersion stress-induced gastric ulcers in rats and histamine-induced gastric and duodenal ulcers in guinea pigs. Shay ulcers and histamine-carbachol-induced duodenal ulcers in rats were not affected by cimetidine. Both ranitidine and cimetidine inhibited the gastric acid output in pylorus-ligated rats (7 hr); the maximal inhibition being 79.6% and 50.7% respectively. The mechanism by which ranitidine inhibits various experimental ulcers might be mainly the inhibition of gastric secretion. Gefarnate at 300 mg/kg (p.o.) significantly inhibited phenylbutazone-induced gastric ulcers in rats but had no effect on other ulcer models.

Acute Disease↗
PubMed1981

[Effects of ranitidine, a new histamine H2-receptor antagonist, on secretagogue-stimulated gastric secretion in rats: comparison with cimetidine (author's transl)].

Antisecretory effects of ranitidine on secretagogue-stimulated gastric secretion in acute fistula rats were studied. Histamine 2HCl (8 mg/kg/hr), pentagastrin (125 micrograms/kg/hr) or carbachol (128 micrograms/kg/hr) was continuously given i.v. by an infusion pump, through the tail vein to acute fistula rats. Gastric secretion was collected hourly for 5 hr and analyzed for its components. Cimetidine was used as a reference drug. Both drugs were given i.v. by a bolus injection in the tail vein 30 min after the injection of each stimulant. Both ranitidine (1 and 10 mg/kg) and cimetidine (10 and 60 mg/kg) significantly (P less than 0.05) inhibited the histamine-stimulated gastric secretion (volume, acid and pepsin output) for 1 to 4 hr. Both ranitidine (10 mg/kg) and cimetidine (60 mg/kg) significantly (P less than 0.05) inhibited the pentagastrin-stimulated gastric secretion for 2 to 3 hr. both ranitidine (10 mg/kg) and cimetidine (10 and 60 mg/kg) markedly inhibited the gastric acid secretion in response to carbachol. However, cimetidine (10 or 60 mg/kg) significantly (P less than 0.05) stimulated the volume and pepsin output by carbachol. We conclude that ranitidine is about 6 times more potent than cimetidine for histamine- or pentagastrin-stimulated gastric secretion and almost equal to cimetidine for carbachol-stimulated gastric acid output in rats.

Animals↗
PubMed1981

[Effects of ranitidine, a new histamine H2-receptor antagonist, on secretagogue-stimulated gastric secretion in Heidenhain pouch dogs (author's transl)].

The effects of ranitidine on gastric secretion stimulated with gastric secretagogues were studied in 6 Heidenhain pouch dogs (both male beagle and mongrel). Cimetidine was used as a reference drug. Either histamine 2HCl (40 micrograms/kg), pentagastrin (2 micrograms/kg) or carbachol (2 micrograms/kg) was given intramuscularly, every 15 min for 120 min. Gastric juice was collected at each 15 min interval and analyzed for volume, acidity and pepsin activity. Either ranitidine (0.3, 1 or 10 mg/kg) or cimetidine (1 or 10 mg/kg), packed in a gelatin capsule, was given orally 60 min before the initial injection of each stimulant. Both ranitidine and cimetidine dose-dependently inhibited histamine- and pentagastrin-stimulated gastric secretion (volume, acid and pepsin output). These agents also inhibited the carbachol-stimulated secretion, but the antisecretory effects were weak as compared with their effects on histamine- and pentagastrin-stimulated secretions. The antisecretory effect of ranitidine on each stimulant is roughly 2 to 17 times more potent than cimetidine on the basis of ED50 (anti-secretory dose which inhibits gastric secretion by 50%). The antisecretory effect of ranitidine (10 mg/kg) on pentagastrin-stimulated secretion was observed even 10 hr after its oral administration.

Animals↗
PubMed1980

Effects of 16, 16-dimethyl prostaglandin E2 methyl ester on aspirin-and indomethacin-induced gastrointestinal lesions in dogs.

The pathogenesis of aspirin- or indomethacin-induced gastric and/or intestinal lesions was studied in dogs. 16,16-Dimethyl PGE2 methyl ester (16-DMPGE2) at 2 or 10 microgram/kg in two divided doses given intramuscularly markedly inhibited gastric lesions produced by orally ingested aspirin at 200 mg/kg/day given twice daily for 1 or 5 days. While 16-DMPGE2 at the same dose also inhibited gastric lesions induced by a single oral administration of indomethacin at 20 mg/kg, gastric lesions including deep antral ulcers, produced by repeated administration of indomethacin, were not affected. Intestinal lesions produced by indomethacin given once, or for 5 or 10 days, were not affected. These results suggest that the lack of engoenous prostaglandins may be involved in the pathogenesis of gastric lesions produced by aspirin and indomethacin given once but may not be involved in the pathogenesis of indomethacin-induced deep lesions in the stomach and intestine.

16,16-Dimethylprostaglandin E2↗
PubMed1979

The mechanism of aggravation of indomethacin-induced gastric ulcers by adrenalectomy in the rat.

Bilateral adrenalectomy markedly aggravated gastric ulcers in rats induced by 5 or 20 mg/kg of indomethacin. The degree of aggravation was much the same in experiments done 1 and 14 days after operation. Pretreatment with prednisolone 10 mg/kg or cortisone acetate 10 mg/kg given subcutaneously significantly suppressed the aggravated ulceration in response to 20 mg/kg of indomethacin in these adrenalectomized rats. Desoxycorticosterone acetate 10 mg/kg, however, had no effect on the aggravation of indomethacin-induced ulcers. Epinephrine 0.1 or 1 mg/kg given subcutaneously markedly suppressed the indomethacin-induced ulcers in adrenalectomized rats. Removal of the adrenal medulla alone did not appreciably influence the development of indomethacin-induced ulcers. These results indicate that the adrenal cortex, particularly the area containing glucocorticoids, plays an important role in suppression of the noxious effect of indomethacin on the rat gastric mucosa.

Adrenal Glands↗