Summary
The minimal concentration of the platelet aggregation principle (Platelet Aggregoserpen-
tin, PAS) necessary to induce platelet aggregation was 10 ng/ml, about one-hundredth
of that of the crude venom. PAS induced the release of platelet factors 3 and 4 from
platelets, but the released platelet factor 3 was easily inactivated by the anti-phospholipid
effect of PAS. Pretreatment of platelets with neuraminidase potentiated PAS-induced
platelet aggregation. PAS-induced platelet aggregation was independent on released
ADP; it could occur in the ADP-removing systems, such as apyrase or a combination
of phosphoenolpyruvate and pyruvate kinase. However, PAS-induced platelet aggregation
could be inhibited by adenine nucleotides and adenosine.
PAS-induced platelet aggregation was inhibited by some anti-inflammatory agents, antimalarial
drugs, local anesthetics, antihistamine and smooth muscle relaxants. After deaggregation
of PAS-treated platelets, thrombin and sodium arachidonate could further induce platelet
aggregation, but ADP and second dose of PAS could not. It is concluded that PAS-induced
platelet aggregation is due to prostaglandin synthesis. Recent literatures on the
mechanism of platelet aggregation were surveyed and the actions of PAS were discussed.