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Biomedical subjects

S Okabe

Publications and source records attributed to S Okabe.

At least 505 records · Page 28Linked to original sources
PubMed1979

[Irritative activity of a new anti-inflammatory agent 4-(p-chorophenyl)-2-phenyl-5-thiazoleacetic acid (CH-800) on the gastrointestinal tract in rats (author's transl)].

A single oral administration of CH-800 induced a dose-dependent irritation of the stomach and intestine. As determined from the UD50 value (the dose inducing ulceration by 50%), the potency of gastric irritation was as follows; indomethacin greater than diclofenac Na greater than ibuprofen greater than aspirin greater than CH-800 greater than phenylbutazone. Repeated administrations of CH-800 for 5 days induced a gastric irritation when given in doses from 3 to 100 mg/kg, however, the response was not dose-related. In contrast, the irritation of intestinal mucosa seen with CH-800 administration was dose-related. The degree of gastric or intestinal irritation seen with dosing of other drugs was as follows; indomethacin greater than diclofenac Na greater than ibuprofen greater than aspirin greater than phenylbutazone or indomethacin greater than CH-800 = diclofenac Na greater than ibuprofen greater than phenylbutazone, respectively. CH-800 given for 5 days significantly delayed the healing of active ulcers and the healed ulcers showed a tendency toward re-ulceration. However, the irritating activity of phenylbutazone, diclofenac Na and ibuprofen was more potent than that of CH-800. Thus, CH-800 appears to have a rather weak irritative activity on the gastrointestinal tract of rats without ulceration, in contrast to other commonly clinically prescribed drugs.

Acetates↗
PubMed1978

Effects of cimetidine on healing of chronic gastric and duodenal ulcers in dogs.

The effects of cimetidine on healing of gastric and duodenal ulcers induced in mongrel dogs were studied. Gastric ulcers were produced by subserosal injection of acetic acid solution and duodenal ulcers by topical application of acetic acid on the serosal surface of the duodenum. Oral treatment with cimetidine, 450 mg/dog/day in three divided doses for 14 days, produced a remarkable acceleration of healing of duodenal ulcers but exerted little influence on gastric ulcers.

Animals↗
PubMed1978

[Irritative activity of antiinflammatory agents, betamethasone 17-valerate, beclomethasone 17, 21-dipropionate, betamethasone 17, 21-dipropionate, or indomethacin on the gastrointestinal tract in rats and dogs (author's transl)].

Irritative effects of three steroidal anti-inflammatory drugs on the gastrointestinal tract of rats and dogs were determined. With either single or repeated subcutaneous administration these drugs dose dependently irritated the gastric mucosa of both species. The intestinal mucosa was less affected. Concomitant oral administration of aspirin or subcutaneous administration of indomethacin revealed an aggravation of aspirin-induced gastric ulcers by betamethasone valerate and inhibition of indomethacin-induced intestinal ulcers by beta-methasone dipropionate. These two steroidal drugs had no noxious effect on healing of chronic gastric ulcers induced in rats and dogs. Betamethasone valerate, however, delayed the healing of gastric ulcer in rats. Indomethacin, a non-steroidal anti-inflammatory drug, also induced serious damage to the gastric and intestinal mucosa both of rats and dogs. Indomethacin ingestion delayed the healing of chronic gastric ulcer in rats but not in dogs. Since both steroidal and non-steroidal drugs induce damage to the gastrointestinal tract, a careful monitoring of the patients' complaints should be carried out when these compounds are used as a systemic treatment. Steroidal drugs used in this study, however, appear to be highly safe from the point of dose inasmuch as they are used as a topical treatment.

Animals↗
PubMed1978

Influence of surgical sympathectomy on gastric secretion and ulceration in rats.

The influences of sympathectomy on gastrointestinal mucosa, gastric secretion, acute or chronic gastric ulcers were studied in rats. Uncer ether anesthesia, sympathectomy was performed by surgical removal of the celiac ganglion. Surgical sympathectomy per se produced no pathological changes in the gastrointestinal tract as determined by macroscopical observation 3, 10 or 20 days after operation. The volume of gastric juice and pepsin output were not influenced by the sympathectomy but gastric acid output was significantly increased in pylorus-ligated rats. The sympathectomy worsened the stress- and the indomethacin-induced ulcer and delayed the healing of chronic gastric ulcers a little but not significantly, and had no deteriorative influence on the reserpine-induced ulcers. In contrast, Shay ulcers, aspirin- or secrotonin-induced ulcers were significantly aggravated by sympathectomy. The loss of H+ ions and gain of Na+ ions in the gastric juice of pylorus-ligated and aspirin-treated rats were not affected by sympathectomy.

Acetates↗
PubMed1978

Strain differences in aspirin-induced gastric ulceration in rats.

We found that there are strain differences in aspirin-induced ulceration in pylorus-ligated rats; the ulcer indices varied, from high to low, in the following order: Donryu greater than Sprague-Dawley greater than Wistar. Several experiments including analysis of gastric contents or ionic flux, determination of serum aspirin esterase activity, absorption of aspirin from the stomach, prothrombin time and hexosamine content in gastric mucosa and juice were performed to elucidate the origin of the differences. A significantly higher acid output in Donryu rats, and higher hexosamine content in the gastric mucosa of Wistar rats were noted. However, it appears unlikely that these factors only contribute to the marked strain difference in aspirin-induced ulcers. The possible different sensitivity of gastric mucosal cell itself to aspirin must be considered.

Animals↗
PubMed1977

Effects of cimetidine and atropine sulfate on gastric secretion and healing of gastric and duodenal ulcers in rats.

Cimetidine, a new histamine H2-receptor antagonist (50 or 100 mg/kg) and atropine sulfate (15 mg/kg) given intraduodenally, markedly inhibited gastric secretion in pylorus-ligated rats. Cimetidine (100 or 200 mg/kg/day) given for 10 or 12 consecutive days orally in two divided doses, significantly promoted the healing rate of both gastric and duodenal ulcers induced in rats. Atropine (30 mg/kg/day) also significantly accelerated the healing of duodenal ulcers but failed to affect gastric ulcers.

Animals↗
PubMed1977

Effects of cimetidine, a histamine H2-receptor antagonist, on various experimental gastric and duodenal ulcers.

The effects of cimetidine, a new histamine H2-receptor antagonist, on the development of experimental gastric and duodenal ulcers were studied. It was found that either by the oral, intraduodenal, or intraperitoneal route this agent had a marked inhibitory activity on stress-, aspirin-, indomethacin-, or histamine-induced gastric ulcers in rats and guinea pigs. The effects of cimetidine on stress-, aspirin-, and indomethacin-induced gastric ulcers were dose-dependent in many cases. Pylorus-ligation uclers, reserpine- or serotonin-induced gastric ulcers were little influenced by cimetidine. Duodenal ulcers induced by continuous infusion of carbachol-histamine were significantly inhibited by a simultaneous infusion of cimetidine. An analysis of gastric contents in pylorus-ligated rats after stressing indicated a decreased volume and acid output as the result of intraduodenal cimetidine treatment. In contrast, cimetidine exerted little influence on gastric secretion in rats treated with aspirin or in guinea pigs treated with histamine. Thus, the mechanism of action of cimetidine in preventing gastric or duodenal ulcers is likely to occur by suppression of gastric secretory function in a duodenal ulcer model but by suppression of other unknown ulcerogenic factors in gastric ulcer models.

Administration, Oral↗
PubMed1977

Influence of aspirin on healing of chronic gastric ulcers in dogs.

Gastric ulcers induced in dogs by transserosal injection of 1 ml of 40% acetic acid healed completely by the 7th week after ulceration and never reulcerated during the observation period up to 12 weeks. Acetic acid ulcers in the active (at 1 week), quiescent (3 weeks) or healed (at 7 weeks) stages were not influenced by the daily administration of aspirin 2 g/dog/day for for 5 consecutive weeks. All examinations were done by gastroscopy in addition to macroscopical and histological observations at autopsy.

Acetates↗
PubMed1977

Effects of metiamide and propranolol on gastric secretion in anesthetized dogs.

The effects of metiamide, a histamine H2-receptor antagonist, and propranolol, a beta-adrenergic blocking agent, on gastric secretion were studied in anesthetized dogs. Metiamide, 1.45 mg/kg i.v., markedly inhibited the gastric secretion induced by a continuous i.v. infusion of tetragastrin (8 microng/kg-hr), histamine dihydrochloride (160 microng/kg-hr), or methacholine bromide (100 microng/kg-hr). Propranolol 0.5 or 1.0 mg/kg i.v. produced a significant potentiation of tetragastrin-induced gastric secretion but no influence of the secretion induced by methacholine. Propranolol at 5 or 10 mg/kg i.v. produced a slight reduction of the tetragastrin-induced secretion and a significant reduction of methacholine-induced secretion. Histamine-induced gastric secretion was not affected by propranolol at either 1 and 10 mg/kg i.v. These findings lend support to the hypothesis that interactions among histamine, gastrin and acetylcholine receptors do occur though the degree would not be the same in all directions.

Animals↗