Morphine enhances gastric mucus synthesis in rats

Ho, Mai M.; Ogle, C. W.; Dai, Soter

doi:10.1016/0014-2999(86)90161-5

Cited by 7 publications

(5 citation statements)

References 10 publications

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“…With higher doses of morphine, despite the dose-dependent inhibition of gastric mu cus, the failure of morphine to induce gas tric damage may be related to the larger decrease in gastric acidity and pepsin out put. Our data are however in contrast with those of Ho et al [1984] showing both a dose-dependent increase in ulcer score and a dose-dependent decrease in acidity by mor phine, and with the results of Ho et al [1986] suggesting a morphine-induced in crease in gastric barrier mucus. These differ ences might depend on variations in experi mental conditions and parameters adopted in these studies.…”

Section: Discussioncontrasting

confidence: 56%

“…It has been proposed that the ulcer ative effect of morphine could be due to inhibitory effects of opiates on gastric blood flow [Morley et al, 1982] and/or a decrease in gastric prostaglandin synthesis [Waisman et al, 1985], As far as the action of morphine on gastric mucus is concerned. Ho et al [1986] have found that morphine enhances the synthesis of gastric mucus in normal rats, in spite of the evidence that the same drug produced gastric mucosal lesions in pylorusligated rats [Ho et al, 1984], It was of interest to investigate the rela tionship between gastric ulceration, hy drochloric acid and pepsin secretion and mucosa-bound mucus in pylorus-ligated rats following central and peripheral administra tion of morphine.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Morphine on Gastric Ulceration, Barrier Mucus and Acid Secretion in Pylorus-Ligated Rats

et al. 1987

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The effects of intraperitoneal (IP) or intracerebroventricular (ICV) administration of morphine on acid and pepsin secretion, gastric ulceration and gastric bound mucoproteins were investigated in pylorus-ligated rats. Morphine, administered IP, produced a dose-dependent inhibition of the gastric secretion volume, acidity, pepsin output and bound mucoproteins. By contrast, the effect of morphine on gastric ulcers was not dose-dependent: a significant increase in gastric lesions was obtained with morphine 5 mg/kg IP. Naloxone IP prevented the effects of morphine on gastric secretory volume, acidity and pepsin output, but not on gastric mucus and ulcer score. ICV administration of morphine induced a dose-dependent inhibition of secretory volume, acidity and ulcer score, whereas no modification of gastric mucus was observed. Naloxone ICV prevented the effects of ICV morphine. Overall results suggest that morphine inhibits gastric secretion through both central and peripheral opioid receptors, whereas the inhibitory effect of morphine on bound mucus appears to be exerted on mucus synthesis through peripheral opioid receptors. This inhibitory effect on barrier mucus accounts at least in part for the gastric ulcerogenic action of morphine.

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Section: Discussioncontrasting

confidence: 56%

Section: Introductionmentioning

confidence: 99%

Effects of Morphine on Gastric Ulceration, Barrier Mucus and Acid Secretion in Pylorus-Ligated Rats

et al. 1987

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“…Gyires et al [ 13] have shown that morphine can also poten tiate indomethacin-induced damage. Opi ates have been shown to decrease mucus secretion in some studies [14], although other studies have shown them to cause an increase [11] and also to decrease gastric blood flow [15]. Fentanyl binds primarily to p-receptors whereas morphine affects k-and possibly 8-receptors as well as p-receptors [16].…”

Section: Discussionmentioning

confidence: 99%

Dose-Dependent Effects of Fentanyl on Indomethacin-Induced Gastric Damage

Playford¹,

Vesey²,

Haldane

et al. 1991

Digestion

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Whilst developing a rat model for studies of gastric protection, we noticed that the anaesthetic agent ‘Hypnorm’, containing the opiate fentanyl 0.315 mg/ml and the butyrophenone fluanisone 10 mg/ml, was itself protective against indomethacin-induced damage: unrestrained animals given indomethacin (20 mg/kg) subcutaneously had an ulcer score of 9 ± 1 mm², compared with 1 ± 1 mm² in animals pre-treated with Hypnorm (0.8 ml/kg) and then given indomethacin (p < 0.01). Further investigation showed this effect to be due to fentanyl-inhibiting gastric acid secretion: doses of fentanyl (90 and 180 μg/kg) which decreased indomethacin-induced damage also caused a rise in intragastric pH from 2.7 ± 0.6 in controls to 5.1 ± 0.8 and 5.0 ± 0.8, respectively. However, the response of fentanyl varied depending on the dose given: fentanyl, 3.6 μg/kg did not affect indomethacin-induced damage, 8 ± 2 vs. 9 ± 1 mm²; fentanyl, 18 μg/kg potentiated damage, 15 ± 4 mm² (p < 0.05), whereas fentanyl, 90 μg/kg and 180 μg/kg decreased damage, 2 ± 1 mm² and 0.1 ± 0.1 mm², respectively (p < 0.01). Neither the butyrophenone haloperidol (8.3 mg/kg) nor the α-adrenergic receptor antagonist phenoxybenzamine (3 mg/kg) protected against indomethacin-induced damage. We conclude that fentanyl affects intragastric pH and can both potentiate and protect against indomethacin-induced damage. Furthermore, the potentiation of gastric damage by fentanyl occurred at doses similar to those used for human anesthesia, so clinical studies are suggested.

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“…These processes, in other words, could provide a 'shield' to damaging agents. The possibility of a role for mucus in partic ular is suggested by recent findings of Ho et al [16] who showed increased mucus pro duction after morphine administration in the rat.…”

Section: Discussionmentioning

confidence: 84%

Protection by Opioids against Gastric Lesions Caused by Necrotizing Agents

Ferri

Speroni²,

Candeletti³

et al. 1988

Pharmacology

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The synthetic opioid met-enkephalin analog [D-Ala², MePhe⁴, Met(0)⁵ol] enkephalin (DAMME) and the opiate morphine injected intraperitoneally to rats at doses of 0.5–2 and 5–20 mg/kg, respectively, showed a protective effect on gastric damage induced by oral administration of necrotizing agents (0.6 NHCl or 0.2 NNaOH solutions, 1 ml/rat). The protection was prevented by naltrexone (10 mg/kg s.c), an opioid antagonist with long-lasting activity. Histological sections of mucosal samples from animals pretreated with morphine (10 mg/kg i.p.) and DAMME (1 mg/kg i.p.) showed less alteration of the columnar epithelium, with a normal glandular structure, than untreated rats. A mediation of prostaglandins is suggested, since indomethacin (10 mg/kg s.c.) significantly reduced the protective effects of opioids.

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Morphine enhances gastric mucus synthesis in rats

Cited by 7 publications

References 10 publications

Effects of Morphine on Gastric Ulceration, Barrier Mucus and Acid Secretion in Pylorus-Ligated Rats

Effects of Morphine on Gastric Ulceration, Barrier Mucus and Acid Secretion in Pylorus-Ligated Rats

Dose-Dependent Effects of Fentanyl on Indomethacin-Induced Gastric Damage

Protection by Opioids against Gastric Lesions Caused by Necrotizing Agents

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