Summary
The relative contribution of platelets to plasminogen activator inhibitor (PA-inhibitor)
activity in blood was investigated. From the difference in PA-inhibitor levels in
platelet-poor plasmas of 12 donors (3 ± 1 U/ml, mean ±95% confidence limits) and in
the corresponding platelet-rich plasmas after induction of platelet aggregation by
collagen, ADP or epinephrine (7 ± 1 U/ml), it may be concluded that a greater amount
of PA-inhibitor in blood is associated with platelets than with plasma. In collagen-stimulated
platelets maximal release of PA-inhibitor and of beta-thromboglobulin (β-TG) was attained
within fifteen seconds, whereas in ADP-stimulated platelets the release of both factors
was slower. In platelet-poor plasma no correlation was found between the level of
PA-inhibitor and that of P-TG. Thus, the PA-inhibitor found in plasma is not derived
from platelets that had been stimulated after blood collection. The rate of complex
formation and the Mr of the principal complexes of radioiodinated tissue-type plasminogen
activator (t-PA) or urokinase (UK), in platelet-poor plasma, in platelet-rich plasma
after platelet aggregation or in an extract of washed platelets was the same. Moreover,
complexes of UK or t-PA with plasmatic PA-inhibitor or with the PA-inhibitor(s) from
platelets bound to immobilized antibodies against bovine endothelial cell-derived
PA-inhibitor. These results show that the PA-inhibitors in plasma and in platelets
are very similar or identical.
Key words
Platelets - Plasminogen activator inhibitor
