The role of platelet prostanoids and dense granule compounds in initial attachment, spreading and aggregation of platelets on collagen substrates.

The role of platelet prostanoids, ADP and 5HT in initial attachment, spreading and aggregation of platelets on collagen substrates (CI, CIII, CIV, CV, CC) was studied. A positive linear correlation was found between thrombi-like aggregate formation on collagen substrates and production of platelet prostanoids. No correlation was established between platelet aggregation and 14C-5HT release. Thrombi-like aggregate formation was completely inhibited by indomethacin and TXA2/PGH2 antagonists (13-APA and BM 13.177). Both 13-APA and BM 13.177 had no effect on platelet spreading, while indomethacin inhibited this process by 25%. The ADP-scavenger system (CP/CPK) inhibited platelet aggregation and spreading by 25-30%. Initial attachment was not influenced by aspirin, indomethacin and CP/CPK. The data obtained indicate that platelet aggregation on collagen substrates is mediated by PGH2 and TXA2 production. These compounds slightly affect the platelet spreading. Both platelet spreading and aggregation on collagen substrates are only partially mediated by ADP and 5HT release. Initial attachment of platelets does not depend on the release reaction and PGH2/TXA2 synthesis.