This looks like certain NSAIDs can also block the inflammatory mediators made from the Mead acid:
Agents Actions Suppl. 1977 ;2 :77-83 PMID: 272845
Effects of anti-inflammatory drugs on the carrageenin-induced hind paw inflammation of rats deprived of endogenous precursors of prostaglandins.
I L Bonta, H Bult
The carrageenin-induced paw oedema was used to study anti-inflammatory drugs in normal rats and in those deprived of endogenous precursors of prostaglandins. The latter condition was achieved by permanently keeping the rats on essential fatty acid deficient (EFAD) food. Indomethacin inhibited the carrageenin-oedema in normal rats, but failed to further suppress the poorly developed delayed phase of the carrageenin-induced inflammation in EFAD rats. In contrast, aspirin exhibited equal inhibition of the carrageenin oedema in both normal and EFAD rats. The anti-inflammatory effect of dexamethasone was also indentical in both normal and EFAD rats. Since in EFAD rats the inflammatory role of an increased output of prostaglandins is of negligible importance, the results with aspirin and dexamethasone shed some doubt on such views, that suppression of the release of prostaglandins alone explains the acute anti-inflammatory effects of these drugs. The inflammatory response of EFAD rats is a model situation appearing to be useful in studying anti-inflammatory mechanisms which, under normal conditions, might be masked by interference with the release of prostaglandins.
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