1982
DOI: 10.1016/0014-2999(82)90168-6
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Indomethacin and paracetamol: Interaction with prostaglandin synthesis in the rat stomach

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1983
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Cited by 11 publications
(6 citation statements)
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“…Paracetamol inhibits the ex vivo production of PGE 2 from mouse brain cells [47]. It also stimulated the production of PGs in the rat stomach [48], but did not reduce urinary excretion of PGE 2 [49]. Mean paracetamol consumption did not differ significantly between the two groups, which may reduce the effect of paracetamol in our study.…”
Section: Discussionmentioning
confidence: 53%
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“…Paracetamol inhibits the ex vivo production of PGE 2 from mouse brain cells [47]. It also stimulated the production of PGs in the rat stomach [48], but did not reduce urinary excretion of PGE 2 [49]. Mean paracetamol consumption did not differ significantly between the two groups, which may reduce the effect of paracetamol in our study.…”
Section: Discussionmentioning
confidence: 53%
“…The effect of paracetamol on PG biosynthesis is variable [47][48][49]. Paracetamol inhibits the ex vivo production of PGE 2 from mouse brain cells [47].…”
Section: Discussionmentioning
confidence: 99%
“…In con trast to nonsteroidal anti-inflammatory drugs (NSAIDs), a previous study has shown that acetaminophen does not induce serious gastrointestinal damage in man [1], In addition, administration of a high dose of acetamino phen (orally or intraperitoneally) has been reported to exhibit a protective effect on gas tric mucosa against various irritants, such as NSAIDs, ethanol and stress [2][3][4], It has been stated that acetaminophen may stimulate prostaglandin Ea (PGE2) synthesis to protect gastric mucosa [5], On the contrary, some reports have suggested that protection by acetaminophen was not attributable to the stimulation of PG synthesis but due to an increase in mucus secretion [3] or to a direct effect on gastric mucosal cells [6], Other studies have reported acetamino phen to possess direct antioxidant actions against free-radical-induced oxidative stress in vitro [7][8][9][10], but it remains to be shown if the in vivo gastric protective effect of acet aminophen is due to its antioxidant effect. Superoxide radicals or hydroxyl radicals have been reported to play important roles in the pathogenesis of gastric erosions induced by ischemia-reperfusion in rats [11][12][13][14], There fore, using this model of acute gastric mucosal injury, we studied whether or not the protec tive effect of acetaminophen against ischemia-reperfusion-induced gastric injury is due to antioxidant or radical scavenging ac tions in vivo.…”
Section: Introductionmentioning
confidence: 99%
“…Previous studies indicate that low levels of acetaminophen exposure increase PG synthesis in rats (van Kolfschoten et al, 1981(van Kolfschoten et al, , 1982Boughton-Smith and Whittle, 1983;Danon et al, 1983), facilitating ovulation (Tsafriri et al, 1972;Clark et al, 1978;Ando et al, 1999) and implantation (Hurst and MacFarlane, 1981;Agrawal and Alvin Jose, 2009). Studies of urinary acetaminophen concentrations in women found no association with fecundability (Smarr et al, 2016).…”
Section: Discussionmentioning
confidence: 99%
“…The most commonly used non-NSAID pain-reliever among US women during the preconception period is acetaminophen (Werler et al, 2005), which has potent analgesic effects but limited antiinflammatory effects (Botting, 2000). Compared with NSAIDs, acetaminophen has weak and varying effects on PG synthesis, with high levels of exposure inhibiting synthesis, and low levels of exposure stimulating synthesis (van Kolfschoten et al, 1981(van Kolfschoten et al, , 1982Boughton-Smith and Whittle, 1983;Danon et al, 1983). In humans, acetaminophen has been shown to slightly reduce the odds of anovulatory cycles (Matyas et al, 2015) and have little effect on female fecundability (Smarr et al, 2016).…”
Section: Introductionmentioning
confidence: 99%