A preliminary study of the inhibiting mechanism of anisodamine on rabbit platelets activated by E. coli endotoxin.
In this study, we observed the endotoxin induced platelet aggregation, 5-HT and beta-g releases, cellular cAMP decrease, and also the changes of morphology and membrane fluidity of platelet. These changes play an important role in septic shock, especially in disseminated intravascular coagulation (DIC) and respiratory distress syndrome (RDS). After anisodamine (654) intervention all the parameters mentioned above were improved to a certain extent. This preliminary study of the inhibiting mechanism of 654 on rabbit platelets activated by ET supports the clinical possibility of using 654 for relieving DIC and RDS.
Xu
S H
SH
Zhu
G J
GJ
Wu
Q X
QX
Chen
H C
HC
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects; D004731:Endotoxins / Q000037:antagonists & inhibitors; D004926:Escherichia coli; D005260:Female; D008297:Male; D008560:Membrane Fluidity / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors; D011817:Rabbits; D012991:Solanaceous Alkaloids / Q000494:pharmacology*
D004731:Endotoxins; D010975:Platelet Aggregation Inhibitors; D012991:Solanaceous Alkaloids; C003922:anisodamine