Difference in mode of action of cimetidine ane gefarnate on endogenous prostacyclin, prostaglandin E2 and thromboxane in rat gastric mucosa.

Nakamura, Hajime; Chono, Shinji; Satoh, Hiroshi; Yamada, Hiroaki; Ono, Tokio; Kobayashi, Kenzo

doi:10.1620/tjem.140.407

Cited by 5 publications

(2 citation statements)

References 26 publications

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“…Prostaglandins that show "cytoprotective" effects against gastric damage induced by nox ious agents (2) have been recognized as im portant defensive factors. It has been sug gested that CIM decreases PG production in the rat (8). On the other hand, Branski et al demonstrated that PG in the gastric mucosa of patients, suffering from duodenal ulcers, was significantly increased after CIM treatment (5).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Cimetidine on Adaptive Cytoprotection by Mild Irritant Dose of HC1 in the Rat Gastric Mucosa

Ota

Hiraishi²,

Terano³

et al. 1991

Japanese Journal of Pharmacology

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ABSTRACT--While cimetidine (CIM) is strikingly effective in inhibiting gastric acid secretion, its effect on the defensive mechanisms of the gastric mucosa has been con troversial. The aims of the present study were to test if administration of CIM at an antisecretory dose is protective against acid-induced injury and to assess its effect on adaptive cytoprotection induced by non-necrotizing concentrations of HCl in rats. A dose of 100 mg/kg of CIM was administered once, or twice a day for 5 days intraperi toneally. To study the effect of CIM on HCl-induced damage, 0.6 N HCl was given orally one hour after the last administration of CIM. To study the effect of CIM on adaptive cytoprotection, 0.35 N HCl was given orally one hour after the last adminis tration of CIM. Fifteen minutes later, 0.6 N HCl was given orally. Thirty minutes af ter the administration of 0.6 N HCI, the stomach was removed and ulcer indices were calculated. Pretreatment with CIM did not prevent 0.6 N HCI induced gastric damage. Prior administration of 0.35 N HCI significantly reduced ulcer indices caused by 0.6 N HCI. Short or long term treatment with CIM did not have significant effects on the reduction of ulcer indices. These results suggest that CIM at an antisecretory dose neither acts as a protective agent nor modulates the protective process of the gastric mucosa.Recently histamine H2 receptor blocking agents (H2 blockers) have been widely used in the therapy of peptic ulcers. While H2 block ers are effective as ulcer-healing agents, the frequency of relapse has been reported to be relatively high (1). On the other hand, pros taglandins (PG) are important defensive agents of the gastric mucosa. Exogenously administered PG prevents gastric damage in duced by necrotizing agents (cytoprotection, 2). Low concentrations of necrotizing agents (mild irritants) also show similar effects against strong irritants by stimulation of en dogenous formation of PG (adaptive cyto protection, 3). The effect of H2 blockers on PG production has been controversial (4-7). H2 blockers might decrease endogenous PG formation or change the response of the gas tric mucosa to mild irritants. The purpose of our study was to assess the effect of short and long term administration of cimetidine at an anti-secretory dose on HCl-induced gastric damage and adaptive cytoprotection.

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Section: Discussionmentioning

confidence: 99%

The Effect of Cimetidine on Adaptive Cytoprotection by Mild Irritant Dose of HC1 in the Rat Gastric Mucosa

Ota

Hiraishi²,

Terano³

et al. 1991

Japanese Journal of Pharmacology

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“…According to Arakawa et al (6), cimetidine administered to rats twice a day for 7 days at a daily dose of 40 mg/kg decreased PGE2 and PGF1a in the gastric mucosal tissue. By con trast, Branski et al (5) reported that the ac cumulation of PGE2 and PGF1a in the biopsy specimens from the stomach of ulcer patients was significantly increased after 4 weeks of cimetidine treatment at a daily dose of 1 g. Okada et al (10) also showed that the PGE2 level in the gastric mucosa of rats exposed to restraint and water-immersion stress was elevated by 25 mg/kg of oral cimetidine.…”

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confidence: 99%

Effects of Cimetidine on Prostanoid Production in the Gastric Corpus Specimens from Rats

Kubota

Sugaya

Hotta

1988

Japanese Journal of Pharmacology

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Abstract-In order to examine the effect of cimetidine on the production of pro stanoids in the stomach mucosa, the amounts of prostaglandin (PG) E2, F1a and thromboxane (TX) B2 were determined after the specimens from the rat stomach corpus were incubated in the presence of cimetidine.Cimetidine significantly stimulated the production of PGE2 in the specimens at a concentration of 10 ,tM, but did not significantly affect the production of PGF1a and TXB2 at concentrations of 1 to 100 11M.

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Biologically active derivatives of polyprenylacetic acids and related compounds (review)

Serebryakov

Nigmatov

1990

Pharm Chem J

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Difference in mode of action of cimetidine ane gefarnate on endogenous prostacyclin, prostaglandin E2 and thromboxane in rat gastric mucosa.

Cited by 5 publications

References 26 publications

The Effect of Cimetidine on Adaptive Cytoprotection by Mild Irritant Dose of HC1 in the Rat Gastric Mucosa

The Effect of Cimetidine on Adaptive Cytoprotection by Mild Irritant Dose of HC1 in the Rat Gastric Mucosa

Effects of Cimetidine on Prostanoid Production in the Gastric Corpus Specimens from Rats

Biologically active derivatives of polyprenylacetic acids and related compounds (review)

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