Inhibitory effects of copper-aspirin complex on platelet aggregation
Abstract
AIM: To study the inhibitory effects of copper-aspirin complex (CuAsp) on
platelet aggregation.
METHODS: With adenosine diphosphate the effects of CuAsp on platelet aggregation
in vitro or in vivo were investigated. Radioimmunoassay and fluorophotometry were
used to measure thromboxane B2 (TXB2) generation from platelets, the levels of
TXB2 and of 6-keto-PGF1 alpha in plasma and the platelet serotonin release
reaction.
RESULTS: In vitro, CuAsp inhibited arachidonic acid (AA)-induced aggregation
(IC50 = 17 mumol.L-1, 95% confidence limits: 9-33 mumol.L-1), the release of 5-HT
(IC50 = 19 mumol.L-1, 95% confidence limits: 10-30 mumol.L-1), and TXB2
generation from platelets (P < 0.05). CuAsp 10 mg.kg-1 i.g. selectively inhibited
AA-induced aggregation, and increased the 6-keto-PGF1 alpha concentration in
plasma while decreased that of TXB2.
CONCLUSION: CuAsp, in vitro or in vivo, shows more potent inhibitory effects on
AA-induced aggregation than aspirin (Asp), related to the inhibition of platelet
cyclooxygenase and the release of active substances from platelets.
Keywords:
platelet aggregation.
METHODS: With adenosine diphosphate the effects of CuAsp on platelet aggregation
in vitro or in vivo were investigated. Radioimmunoassay and fluorophotometry were
used to measure thromboxane B2 (TXB2) generation from platelets, the levels of
TXB2 and of 6-keto-PGF1 alpha in plasma and the platelet serotonin release
reaction.
RESULTS: In vitro, CuAsp inhibited arachidonic acid (AA)-induced aggregation
(IC50 = 17 mumol.L-1, 95% confidence limits: 9-33 mumol.L-1), the release of 5-HT
(IC50 = 19 mumol.L-1, 95% confidence limits: 10-30 mumol.L-1), and TXB2
generation from platelets (P < 0.05). CuAsp 10 mg.kg-1 i.g. selectively inhibited
AA-induced aggregation, and increased the 6-keto-PGF1 alpha concentration in
plasma while decreased that of TXB2.
CONCLUSION: CuAsp, in vitro or in vivo, shows more potent inhibitory effects on
AA-induced aggregation than aspirin (Asp), related to the inhibition of platelet
cyclooxygenase and the release of active substances from platelets.