Comparison of the mediator release from platelets and the development of acute inflammation in rats which lack prostaglandin precursors.

Rat platelet rich plasma (PRP) generates prostaglandin endoperoxide-like activity, thromboxane A2 (TXA2) and stable prostaglandins (PGs) after collagen addition. Of the stable PGs, PGE is the main product and its formation is related to the dose of collagen. Indomethacin and eicosatetraynoic acid (TYA), both cyclo-oxygenase inhibitors, inhibit TXA2 and PGE formation simultaneously. PRP of essential fatty acid deficient (EFAD) rats, however, generates far less PG-endoperoxide like activity, TXA2 and PGE, though the release of serotonin (5-HT) is unaltered. In normal rats a marked inhibition of the cyclo-oxygenase by TYA also has no effect on 5-HT release. For these 2 reasons the role of PG endoperoxides and TXA2 seems to be unimportant for the 5-HT release reaction. The diminished biosynthesis of PGs and TXA2 in EFAD PRP is not due to an impaired cyclo-oxygenase activity since addition of AA causes an equal formation of PGE in both types of PRP. The use of platelets as in-vitro model for testing anti-inflammatory activity of drugs is discussed. The results, obtained with platelets support the hypothesis that the main reason for the decreased acute inflammatory reaction in EFAD rats is a diminished supply of endogenous PG precursors.