Summary
Human platelets labeled with 51Cr were used to determine the contribution made by platelet lysis to the platelet
release reaction and platelet aggregation induced by rabbit antihuman platelet serum
(APS) and equine antihuman thymocyte globulin (ATG). Platelets were tested in both
plasma (PRP) and non-plasma containing media. Antibodies directed against platelets,
either as APS or ATG, induced significant amounts of platelet release and aggregation,
as well as some degree of lysis, in the absence of complement. The presence of complement
increased platelet lysis and aggregation, but not the release reaction. Non-immune
horse gamma globulin produced different responses depending upon whether platelets
were investigated in PRP or non-plasma containing media. Aggregation was seen in the
latter but not the former. These differences can be explained by the presence of plasma
components which prevent non-specific immune complexes from causing platelet aggregation.
Since platelets in vivo are always in a plasma medium, one must be wary of utilizing
data from platelet studies in synthetic plasma-free media as the basis of explaining
clinical events. These observations demonstrate at least two, and possibly three,
different mechanisms whereby ATG could activate platelets causing thrombotic complications
and thrombocytopenia, i.e., via 1) specific and, 2) non-specific non-lytic pathways
and 3) a lytic pathway.
