Prostaglandins and acute inflammatory reactions : studies on rat platelets and carrageenin-induced paw edema
Despite the vast amount of accumulated data on inflammation, there are still large gaps in our knowledge about the pathways involved in the development of an inflammatory response (see Ebert & Grant, 1974). Thus, effective therapy of several chronic inflarmnatory diseases is, at this moment, beyond medical capabilities. For the control of the inconvenient and painful symptoms of diseases like rheumatoid arthritis, physicians still have to rely on drugs which have largely been developed empirically and are used in an empirical way (eg. Kaye & Pemberton, 1976). The mode of action of several of these "anti-inflammatory drugs", Hhich often only relieve anoying symptoms of the disease, has for a long time been shrouded in mystery. Only recently, Vane and co-Harkers (1971) discovered the main biochemical action of a group of these drugs, kno.vn as non-steroidal anti-inflammatory drugs (NSAIDs), of which aspirin (acetylsalicylic acid) is the most familiar representative. It appeared that aspirin-like drugs suppress prostaglandin (PG) biosynthesis, both in vitro and in vivo (82,233,254). This led to the concept that inhibition of PG release explains the anti-inflammatory effect of NSAIDs.