Summary
The effects of polylysine on human platelets have been examined in citrated platelet-rich
plasma (PRP) and in suspensions of washed platelets in various media. In PRP, polylysine
caused aggregation after a lag phase. Heparin inhibited this completely. At certain
concentrations of polylysine, two phases of aggregation occurred, the second being
associated with release of 14C-serotonin from prelabelled platelets; this phase was inhibitable with prostaglandin
E1, acetylsalicylic acid, sulphinpyrazone, adenosine, apyrase, or creatine phos- phate/creatine
phosphokinase. Polylysine-induced release also occurred in PRP with EDTA or hirudin
as anticoagulant. In suspensions of washed platelets in Tyrode solution containing
0.35% or 4% albumin, or 1% gelatin, polylysine caused immediate platelet-to-platelet
adherence and very little release of 14C-serotonin or platelet lysis. Heparin inhibited aggregation, but acetylsalicylic
acid, prostaglandin E1, adenosine, apyrase, creatine phosphate/creatine phosphokinase or EDTA did not. In
a modified Tyrode-albumin medium containing 1 mM magnesium but no calcium, polylysine-induced
aggregation was associated with the release of 14C-serotonin which could be inhibited by acetylsalicylic acid or indomethacin; this
is similar to the effect of ADP in this medium. In Tyrode solution without albumin
or gelatin, polylysine-induced platelet aggregation was associated with release of
a large percentage of 14C-serotonin, together with as much as 18% lysis; indomethacin inhibited this release
reaction.