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Firstly, the studies by Graham and Scott have shown that paracetamol really inhibited prostaglandin synthesis in well-functioning cells, however, it did not exert the acetaminophen same effect in the tissue/cell homogenate, where the concentration of arachidonic acid is low (35) .
Secondly, paracetamol has been found to have an inhibitory impact on COX-1 and COX-2 activity in peripheral tissues, although not to the same extent, since a stronger effect was always observed in relation to COX-2, especially in the cells of acetaminophen shelf life acetaminophen dosing guidelines fda acetaminophen arthritis side effects the vascular endothelium .
In numerous academic textbooks including those published during the acetaminophen price acetaminophen journal acetaminophen bleeding risk acetaminophen kidney damage last decade, the central mechanism of paracetamol action has been discussed emphasizing its weaker inhibitory effect on the cyclooxygenase activity and prostaglandin production as compared to NSAIDs .
The early study by Flower and Vane from 1972 in the acetaminophen prestige magazine Nature announced the mechanism of paracetamol activity even in its title: îInhibition of prostaglandin synthetase in brain explains the antipyretic activity of paracetamol (4-acetamidophenol)î (18) .
Scientific prestige of the future Nobel prize winner, acetaminophen John R .
Vane, was so high that despite later published articles, which did not completely confirm the original results of acetaminophen the British researchers (19-21) that study was still citied and its results were considered the substantial basis of the mechanism of paracetamol action for many pharmacologists and doctors .
Flower and Vane indicated that prostaglandin production in the brain was acetaminophen 10-fold more sensitive to paracetamol action than in the spleen (18) .

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