Platelet prostanoids in interaction of platelets with collagen substrates. I. Activation of platelets by surfaces coated with different types of human collagen.

We have studied the interaction of human platelets with surfaces coated with human type I, III, IV, and V collagen (CI, CIII, CIV, and CV). It was established using scanning electron microscopy that the reactivity of the collagen substrates for platelets varies widely. On CV, only the initial attachment of platelets takes place; spreading actively goes on CIV while on CI and CIII, along with spreading, the formation of multilayer thrombi-like platelet aggregates occurs. The production of malondialdehyde induced by the interaction of platelets with CI and CIII substantially exceeds that stimulated by CIV and CV. Indomethacin practically completely inhibits the formation of thrombi-like aggregates but only by 25% inhibits platelet spreading. An ADP-scavenger creatine phosphate/creatine phosphokinase inhibits the formation of thrombi-like aggregates and platelet spreading by 25-30%. The obtained data demonstrate that: (i) the formation of thrombi-like aggregates on CI and CIII is mediated mainly by the synthesis of platelet prostanoids, and not by the ADP release; (ii) the spreading of platelets on CIV, CIII, and CI is only partially mediated by prostanoid synthesis and ADP release which suggests a participation of other mechanisms in this process.