Oxygen was supplied in these studies in marked excess of tissue requirements, but when Harper, Ledingham, and McDowall (1965) caused cerebral underperfusion by haemorrhage they found that high arterial oxygen tensions no longer reduced cerebral
Effect of etodolac on the prostaglandin concentrations in the kidney of the normal rat
โ Scribed by Dr. David K.H. Lee
- Publisher
- John Wiley and Sons
- Year
- 1986
- Tongue
- English
- Weight
- 440 KB
- Volume
- 9
- Category
- Article
- ISSN
- 0272-4391
No coin nor oath required. For personal study only.
โฆ Synopsis
Lee, D.K.H.: Effect of etodolac on the prostaglandin concentrations in the kidney of the normal rat. Drug Dev. Res. 9:305-311, 1986.
The effect of acute and subchronic dosing with etodolac on the renal PGE2 and 6-keto-PGF,, concentrations in the normal rat were studied. Etodolac and other nonsteroidal antiinflammatory drugs (NSAIDs) were administered orally, at equieffective antiinflammatory doses, to normal rats either as a single dose or as seven daily doses. Whole kidney prostaglandin (PG) concentrations were measured. In the acute study, etodolac (3 mg/kg) did not significantly lower the PGE2 levels for up to 4 hr postdosing. In contrast, naproxen (3 mg/kg) and piroxicam (0.5 mg/kg) significantly decreased the PGE2 levels to about 20% and 60% of control, respectively. Similar reductions in 6-keto-PGF1, concentrations were observed. In the subchronic study, etodolac (3 mglkglday) did not lower either PGE2 or 6-keto-PGF1, concentrations whereas naproxen (3 mg/kg/day), piroxicam (0.5 mg/kg/day), indomethacin (1 mg/kg/day), and aspirin (300 mg/kg/day) significantly decreased both PGs. In both studies, the effect of etodolac was significantly different from that of the NSAIDs. It is concluded that etodolac possesses only a very weak capacity to lower renal PGs, and therefore is unlikely to cause any renal complications related to PG biosynthesis inhibition.
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