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The concept regarding COX-dependent central mechanism of paracetamol action acetaminophen has not stood the test of time (29) .
Firstly, the studies by Graham and Scott have shown that paracetamol really inhibited prostaglandin acetaminophen synthesis in well-functioning cells, however, it did not exert the 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 acetaminophen gpi a5 acetaminophen metabolite side effects hydrocodone acetaminophen 5 325 qualitest was always observed in relation to COX-2, especially in the cells of the vascular endothelium .
In numerous academic textbooks including those published during the last decade, the central mechanism of paracetamol action has been discussed emphasizing its weaker inhibitory effect on the cyclooxygenase activity and acetaminophen prostaglandin production as compared to NSAIDs .
The early study by Flower and Vane from acetaminophen 1972 in the 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 (1Cool .
Scientific prestige of the future acetaminophen side effects dry mouth acetaminophen dosage for 22 lbs acetaminophen max single dose Nobel prize winner, John R .
Vane, was so high that despite acetaminophen oxycodone dosage acetaminophen ld50 tramadol hcl acetaminophen side effects later published articles, which did not completely confirm the original results of 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 .

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