The effects of E and A prostaglandins on gastric mucosal blood flow and acid secretion in the rat

Main, I H; Whittle, Brendan J.R.

doi:10.1111/j.1476-5381.1973.tb17253.x

Cited by 153 publications

(35 citation statements)

References 18 publications

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“…The possibility that PGs exert cyto protection through changes in gastric mucosal blood flow (GMBF) is controversial, as the action of PGs on vascular beds differs with each type, i.e., PGE2 is a peripheral vasodilator and PGF2 is a vasoconstrictor. Although the effect of PGE2 on gastric mucosal blood flow has been reported, the results are not consistent (2,(5)(6)(7)(8). On the other hand, the effect of PG F2.…”

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confidence: 45%

Effect of prostaglandins on mucosal blood flow and aspirin-induced damage in the canine stomach.

Inatomi

Maki

1983

Jpn.J.Pharmacol

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Abstract-This study deals with the action in anesthetized dogs of prostaglandin E2 and F20 given into the celiac artery and the femoral vein on gastric mucosal blood flow and on gastric mucosal damage induced by aspirin. In the non-stimulated stomach , infusion of prostaglandin E2 or F2 into the celiac artery resulted in a marked increase in mucosal blood flow and a sustained decrease, respectively. In contrast, an infusion of pro staglandin E2 into the femoral vein produced a decrease in mucosal blood flow , whereas prostaglandin F21 produced a biphasic response: a transient increase followed by a decrease. It was observed that intravenously infused prostaglandin E2, while reducing mucosal blood flow, significantly diminished mucosal lesions, altered transmucosal potential differences and H+ back-diffusion induced by a topical application of aspirin. The findings indicate that the action of prostaglandins on gastric mucosal blood flow alters depending on the route of administration and that prostaglandins seem to exert gastric cytoprotection through mechanisms other than an increase in mucosal blood flow.

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confidence: 45%

Effect of prostaglandins on mucosal blood flow and aspirin-induced damage in the canine stomach.

Inatomi

Maki

1983

Jpn.J.Pharmacol

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“…PGE2 inhibits acid secretion in vivo (Main & Whittle, 1973) and also in vitro as measured by ['4C]-AP uptake in isolated gastric cells of dog (Soll, 1980;Skoglund et al, 1982), rabbit (Levine et al, 1982) and rat (Schepp et al, 1983b). In rat cells, PGE2 caused a concentration-dependent inhibition of the histamine (10-4moll-')-stimulated AP uptake.…”

Section: Resultsmentioning

confidence: 99%

Prostaglandin formation by isolated gastric parietal and nonparietal cells of the rat

Postius

Ruoff

Szelenyi

1985

British J Pharmacology

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Rat gastric cells isolated by pronase and subdivided by Percoll into 3 fractions (F1, F2, F3) were used to study prostaglandin E2 (PGE2) formation and, as an indirect measure of parietal cell H+ production, [14C]‐aminopyrine uptake. Cells that had not been fractionated, with 20 to 25% parietal cells, contained at 0°C 1.7 ± 0.35 (s.e.mean) ng PGE2 108 cells−1. During incubation at 37°C these cells steadily synthesized up to 4.36 ± 0.73 ng PGE2 108 cells−1 from endogenous substrate. Indomethacin in concentrations higher than 10−6moll−1 inhibited this basal formation completely, but 10−4moll−1 did not reduce the cellular PGE2 level below 1.4 ± 0.2 ng 108 cells−1. Arachidonic acid in concentrations higher than 10−5moll−1 evoked an abundant formation of PGE2, and 10−4moll−1 built up a plateau of over 7.5 ± 1.65 ng PGE2 108 cells−1 within 15 min. PGE2 formation in cell fractions increased significantly with the number of parietal cells per assay tube. Indomethacin (10−8 to 10−4moll−1) did not influence the histamine‐stimulated uptake of [14C]‐aminopyrine, while arachidonic acid (10−5 to 10−4 moll−1) inhibited this process. PGE2 formation in response to arachidonic acid was prevented by indomethacin, but the inhibition of aminopyrine uptake by arachidonic acid could not be prevented by indomethacin. The data suggest that isolated gastric cells of the rat sustain constant PGE2 synthesis in vitro, which is more pronounced in parietal than in mucosal and chief cells. PGE2 may exert different effects within distinct gastric cell types.

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“…An increase of mucus, HCO3 secretion, or mucosal blood flow has been proposed as the possible explanation (25)(26)(27), but these factors, either alone or in combination, cannot account for the occur rence of lesions in a specific shape and site: the "band-like" lesions confined to the crest of the rugae in the stomach.…”

Section: Discussionmentioning

confidence: 99%

Cytoprotective Action of Mast Cell Stabilizers against Ethanol-Induced Gastric Les ons in Rats

Takeuchi¹,

Nishiwaki²,

Okabe³

1986

Japanese Journal of Pharmacology

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Abstract-We examined the effects of FPL-52694 and disodium cromoglycate (DSCG), mast cell stabilizers, on HCI ethanol-induced gastric lesions in rats and investigated the factors involved in their protection.Oral (p.o.) administration of 1 ml of HCI ethanol (60% in 150 mM HCI) induced linear hemor hagic lesions in the gastric mucosa within 1 hr. FPL-52694 (1-30 mg/kg), given both p.o. and intraperitoneally (i.p.), prevented these lesions in a dose-related manner. DSCG (3-30 mg/kg) also dose-dependently reduced the formation of these lesions when this agent was given i.p. The protective effects of these drugs on HCI-ethanol induced lesions were significantly attenuated by pretreatment with indomethacin (5 mg/kg, s.c.).Both gastric acid secretion and transmucosal potential difference were significantly reduced by topical application of FPL-52694 (>10 mg/kg), but were not affected by i.p. administration of FPL-52694 and DSCG. On the other hand, gastric motor activity measured as intraluminal pressure recordings was sig nificantly inhibited for 2 hr by both FPL-52694 (p.o. and i.p.) and DSCG (i.p.), and these effects were also significantly antagonized with prior administration of indomethacin.A significant relationship was found between the effects of these two drugs on the lesion index and the motility index (r: 0.9214, P<0.01), but not other factors.These results suggest that mast cell stabilizers such as FPL-52694 and DSCG protect the gastric mucosa against HCI-ethanol through a systemic action, probably mediated with endogenous prostaglandins. Although the mechanism of cytoprotection remains unknown, this property may be related to their inhibitory effects on gastric motor activity.

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The effects of E and A prostaglandins on gastric mucosal blood flow and acid secretion in the rat

Cited by 153 publications

References 18 publications

Effect of prostaglandins on mucosal blood flow and aspirin-induced damage in the canine stomach.

Effect of prostaglandins on mucosal blood flow and aspirin-induced damage in the canine stomach.

Prostaglandin formation by isolated gastric parietal and nonparietal cells of the rat

Cytoprotective Action of Mast Cell Stabilizers against Ethanol-Induced Gastric Les ons in Rats

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