The release of PGF1alpha and PGF2alpha from superfused blood platelets was studied by the combined use of two radioimmunoassay systems with different specificities. PGF1alpha only accounted for approximately 30% of the total immunoreactivity. A substantially similar pattern of release was obtained with platelets of rat and human origin, although the latter released considerably lower amount of both compounds. Indomethacin, Femoprofen, Ditazole and Aspirin all inhibited PGF2alpha release from rat platelets in descending order of potency. Hydrocortisone was partically inactive. The release of PGF1alpha and PGF2alpha was inhibited to the same extent by both Indomethacin and Fenoprofen. Moreover, a quite similar inhibitory effect by the same drug on rat and human platelets was found in preliminary experiments. In agreement with a previous similar finding, Aspirin displayed a higher inhibitory activity than that reported in other tissues. The use of superfused platelets seems to provide a simple and reproducible model for studying pharmacologic influences upon PG formation.
Animals Anti-Inflammatory Agents, Non-Steroidal