It was revealed that the coagulo-fibriolytic system in severe toxemia of pregnancy showed chronic DIC. But platelet function which included platelet release reaction was not completely studied in severe toxemia of pregnancy. ADP induced platelet aggregation was decreased in those cases, and especially in eclampsia, platelets failed to be aggregated by ADP. To reveal the mechanism of these phenomena, the following study was performed. METHODS Platelet count, ADP induced platelet aggregation, beta-thromboglobulin (beta-TG), antithrombin III (ATIII), and fibrin/fibrinogen degradation products (FDP) were determined during pregnancy, labor, puerperium, and in severe toxemia. RESULTS 1. Platelet count, ADP induced aggregation, ATIII were decreased and beta-TG was increased in severe toxemia and also in the very early period of puerperium, significantly. 2. There was no significant correlation between FDP and ADP induced aggregation. ADP induced aggregation was not inhibited by FDP in vitro at the final concentration of less than 720 micrograms/ml. This suggests that thrombin formation occurs in vivo, in toxemia and in a moment at a very early stage of puerperium, because of high beta-TG level and low ATIII level. But there may be numerous number of platelet which remains reversible. The reduction in the ADP induced platelet aggregation cannot be due to FDP, but may be due to an increased number of exhausted platelets.