Thromb Haemost 1986; 55(02): 201-205
DOI: 10.1055/s-0038-1661522
Original Article
Schattauer GmbH Stuttgart

Studies on the Release of a Plasminogen Activator Inhibitor by Human Platelets

E K O Kruithof
The Hematology Division, Department of Medicine, University Hospital Center, CHUV, Lausanne, Switzerland
,
C Tran-Thang
The Hematology Division, Department of Medicine, University Hospital Center, CHUV, Lausanne, Switzerland
,
F Bachmann
The Hematology Division, Department of Medicine, University Hospital Center, CHUV, Lausanne, Switzerland
› Author Affiliations
Further Information

Publication History

Received 22 October 1985

Accepted 30 January 1986

Publication Date:
18 July 2018 (online)

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.

 
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