Activated platelets play an important part both in the formation of the platelet plug aud as a catalytic surface for the plasma coagulation factors. We have earlier shown that activation of platelets in whole blood collected without anticoagulauts shortens the clotting time by approximately 50%. Here, we examine the involvement of TF, factor XII and factor XI in this platelet-dependent coagulation acceleration.
Addition of an antibody against tissue factor did not prolong the clotting times for blood samples with platelet activators such as TRAP-6 or a collagen related peptide (CRP), nor for samples with only buffer added. Addition of com trypsin inhibitor (CTI) to inhibit fXIIa prolonged the clotting times by 21% for samples with eRP added. In samples with only buffer or with TRAP-6, en prolonged the clotting times by around 50%. Simultaneous addition of en and anti-TF did not cause any fnrther prolongation.
Addition of a polyclonal antibody against factor XI caused a more marked prolongation of the clotting times, especially for TRAP-6 and buffer containing samples, but also for CRP.
Only small amounts of thrombin-anti-thrombin (TAT) complexes were found in fresh blood samples directly after blood sampling, same amounts as described for blood down directly into tubes with anticoagulants. We cannot exclude the possibility that these small amounts could activate factor XI on the platelet surface, but that cannot explain the shortened clotting times and increased amounts of TAT found in samples with CRP added. The nature of this platelet-dependent coagulation amplification will be addressed in coming studies.