Rabbit Platelet Injury by Soluble Antigen and Antibody

Abstract

Abstract Platelet aggregation induced by soluble antigen and antibody unrelated to the platelet membrane in heparinized plasma has been shown to be diphasic. The first wave of aggregation, which is complement- and divalent-cation-dependent, precedes the release of both vasoactive amines and adenosine diphosphate (ADP), is unaffected by the presence of 10 mM adenosine monophosphate (AMP), and coincides in onset with changes in the surface characteristics of the platelets detectable by retention of the platelets on glass bead columns. The second wave of aggregation is accompanied by release of platelet ADP and is totally inhibited by the presence of 10 mM AMP. Release of platelet serotonin occurs well after the second wave of aggregation. Citrate inhibits the second wave of aggregation and the release of both ADP and serotonin. It is postulated that the first wave is due to complement coating of the platelet membrane, which induces membrane injury and release of endogenous platelet materials in heparinized but not in citrated plasma. The second wave of aggregation is mediated by ADP released from the platelet. The first wave of platelet aggregation, which requires only the first four components of complement, clearly precedes and is separable from release of endogenous platelet materials, which requires at least six complement components.