title: [Pharmacological deaggregation of platelet aggregation].
abstract: Antagonists of increasing concentrations were added to PRP which had exhibited irreversible aggregation and the extent of deaggregation was determined. Several classes of platelet antagonists with different mechanisms have been undertaken to reverse platelet aggregation induced by ADP, collagen, arachidonic acid, U46619 and PAF. The results indicate that maintenance of platelet aggregation is a complex phenomenon involving multiple mechanisms which depend on agonists. Maintenance of ADP induced aggregation requires exogenous calcium and active intracellular calcium mobilization. Active intracellular calcium mobilization appears to be essential for maintaining aggregation by PAF, U46619 and arachidonic acid. But additional pathway may be operative in maintaining collagen-induced aggregation. Calmodulin inhibitors with multiple actions are effective deaggregators. Calmodulin plays a role in maintaining platelet aggregation. The present study indicates that the ability of various antagonists to reverse platelet aggregation is closely related to three factors: 1) agonists used to stimulate platelet, 2) the time period following the initiation of platelet aggregation and 3) the kinds of antagonists used.
authors.forename: J Q
authors.initials: JQ
authors.lastname: Pan
authors.forename: Z N
authors.initials: ZN
authors.lastname: Zhang
mesh_terms: D002118:Calcium / Q000494:pharmacology; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*
chemical_list: D010975:Platelet Aggregation Inhibitors; D002118:Calcium