Abstract
Smith & Willis (1970) showed that aggregating platelets release, among other products, prostaglandins of the E and F type. Shortly afterwards it was shown that aspirin-like drugs inhibit prostaglandin biosynthesis (Vane, 1971; Ferreira, Moncada & Vane, 1971; Smith & Willis, 1971) and as a result the general theory was proposed (Vane, 1971) that this enzyme inhibition accounts for the anti-inflammatory effects (and perhaps the side effects) of aspirin-like drugs. Since then, substantial evidence to support this theory has accumulated and it is now widely accepted that the analgesic, anti-pyretic and anti-inflammatory effects of aspirin-like drugs are mediated via inhibition of prostaglandin biosynthesis (Vane, 1976; Moncada & Vane, 1979a).
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Moncada, S., Vane, J.R. (1980). The Pharmacology and Clinical Potential of Prostacyclin. In: Turner, P., Padgham, C., Hedges, A. (eds) Clinical Pharmacology & Therapeutics. Palgrave Macmillan, London. https://doi.org/10.1007/978-1-349-05952-2_3
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