Dödligt virus från Kina orsakar panik (SARS-CoV-2, COVID-19)

It is surprising that after more than 100 years, the exact mechanism of action of paracetamol remains to be determined. There is evidence for a number of central mechanisms, including effects on prostaglandin production, and on serotonergic, opioid, nitric oxide (NO), and cannabinoid pathways, and it is likely that a combination of interrelated pathways are in fact involved. A few of these are outlined below.1

There is evidence for a number of central mechanisms, including effects on prostaglandin production, and on serotonergic, opioid, nitric oxide (NO)

An alternative suggestion was that, unlike NSAIDS, which act on COX-1 and -2, paracetamol may act on a discrete COX-1 splice variant (initially thought to be a distinct isoenzyme, COX-3). This COX-1 variant was thought to be active in the central nervous system, rather than at the site of injured or inflamed tissue, such that inhibition by paracetamol here would explain its lack of anti-inflammatory and anti-platelet activity, whilst still affording it highly effective analgesic and antipyretic properties. However, the original work for this was performed on canine tissue, in which the COX-1 splice variant retains a COX-like action; in humans, however, the expressed protein has no role in the physiology of prostaglandins.