Effects of heparin and alpha 1-acid glycoprotein on thrombin or Activated Thrombofax Reagent-induced platelet aggregation and clot formation.

alpha 1-Acid glycoprotein (AAG) obtained from ascites and/or pleural fluids exhibited anti-heparin effects in platelet-poor plasma when evaluated by activated partial thromboplastin (Activated Thrombofax Reagent) and heparin-thrombin clotting time assays. An anti-heparin effect for AAG was also demonstrable in platelet-rich plasma (PRP) challenged with thrombin, but only over a limited range of heparin concentrations; at elevated heparin concentrations, and only in the presence of AAG, both platelet aggregation and clot formation were substantially inhibited. However, no detectable anti-heparin effect was observed following challenge of PRP with Activated Thrombofax Reagent; indeed, the anti-coagulant effect of heparin appeared synergistically amplified in these systems containing AAG, and AAG exhibited platelet pro-aggregate and pro-coagulant properties in the absence of heparin. The platelet pro-aggregating activity of AAG, though independent of heparin, appeared to require the onset of the coagulation cascade prior to the generation of thrombin; in the absence of such initiation, AAG remained a potent inhibitor of platelet activation.