Salicylic acid fails to inhibit generation of thromboxane A2 activity in platelets after in vivo administration to the rat.
Arachidonic acid-induced aggregation of rat platelets and the accompanying generation of thromboxane A2 activity were inhibited by aspirin, whereas 20 times higher doses of salicylic, gentisic and salicyluric acids were inactive. Salicylic acid administered to the rats before aspirin prevented the inhibition of the cyclo-oxygenase-mediated effects of arachidonic acid. These results do not support the hypothesis that the anti-inflammatory activity of salicylic acid is due to inhibition of prostaglandin systhetase (cyclo-oxygenase) by an unknown metabolite and indicate that salicylic acid displays an anti-inflammatory activity independent inhibition of prostaglandin biosynthesis.
Salicylic acid fails to inhibit generation of thromboxane A2 activity in platelets after in vivo administration to the rat. Arachidonic acid-induced aggregation of rat platelets and the accompanying generation of thromboxane A2 activity were inhibited by aspirin, whereas 20 times higher doses of salicylic, gentisic and salicyluric acids were inactive. Salicylic acid administered to the rats before aspirin prevented the inhibition of the cyclo-oxygenase-mediated effects of arachidonic acid. These results do not support the hypothesis that the anti-inflammatory activity of salicylic acid is due to inhibition of prostaglandin systhetase (cyclo-oxygenase) by an unknown metabolite and indicate that salicylic acid displays an anti-inflammatory activity independent inhibition of prostaglandin biosynthesis.