The rat model of blood stasis syndrome was caused by subcutaneous adrenaline injection incorporated with ice-bathing.We studied the effects of the active fractions of Danshen and Sanqi

i.e.salvianolic acid B(Sal.B)and Rg

on platelet aggregation

platelet adhesion

TXA2 and PGI2 in rat model of blood stasis syndromes.The results indicated that compared with normal rats

the platelet adhesion and ADP-induced platelet aggregation were markedly increased.However

the plasma levels of TXB

6-keto-PGF1α and ADP-induced platelet products of TXB2 and 6-keto-PGF1α in abdominal aorta were not markedly affected in the model rats.Sal.B and Rg significantly inhibited the increase in platelet adhesion and ADP-induced platelet aggregation in the model rats.Sal.B and Rg also markedly increased the plasma levels of TXB2

6-keto-PGF1α and ADP-induced platelet production of TXB2 and 6-keto-PGF1α in abdominal aorta of the model

but had little effect on the ratio of TXB2/6-keto-PGF1α.The results indicated that the blood stasis syndrome model was established successfully.We inferred that the changes in platelet aggregation and platelet adhesion might not be related with TXA2-PGI2.Moreover

the other conclusion is that the inhibition effects of Sal.B and Rg of Danshen and Sanqi in Fufangdanshen prescription on platelet aggregation and adhesion might be closely related to its promotive effect on the release of 6-Keto-PGF1α in the rats.