[A preliminary study of the inhibiting mechanism of anisodamine on rabbit platelets activated by E. coli endotoxin].

Bacterial endotoxin binds to platelets and causes platelet aggregation, thrombocytopenia, increase in thromboxane A2 production, serotonin release and increase in the generation of platelet factor 3 procoagulant activity. These effects have been demonstrated in a variety of animal species. Much evidence has shown that such changes may participate in the pathogenesis of DIC and RDS in septic shock. The anisodamine (654) antishock effect has been studied from different angles for more than 20 years, with its effect on the cardiovascular system, including the microcirculation, being demonstrated. But few reports concerning its effect on platelet function have emerged. In this study, the effect of anisodamine on rabbit platelet aggregation, release, morphological changes, cellular cAMP, and membrane lipid fluidity induced by E. coli endotoxin were studied both in vivo and in vitro. After anisodamine intervention, all of these parameters improved to a certain extent. The possible protective mechanisms of anisodamine on platelets both in vivo and in vitro are discussed.