Thromb Haemost 1991; 65(04): 389-393
DOI: 10.1055/s-0038-1648158
Original Article
Schattauer GmbH Stuttgart

Stimulation of Plasmin Activity by Aspirin

Ariel Milwidsky
1  The Department of Obstetrics and Gynecology, Hadassah University Hospital, Mount Scopus, Jerusalem, Israel
Zvendana Finci-Yeheskel
2  The Department of Clinical Biochemistry, Hadassah University Hospital, Mount Scopus, Jerusalem, Israel
Michael Mayer
2  The Department of Clinical Biochemistry, Hadassah University Hospital, Mount Scopus, Jerusalem, Israel
› Author Affiliations
Further Information

Publication History

Received: 08 May 1990

Accepted after revision 16 November 1990

Publication Date:
02 July 2018 (online)


This study demonstrates an enhancing effect of aspirin on the amidolytic activity of plasmin. The stimulation of plasmin by aspirin was concentration-dependent and was attained at aspirin concentrations above 2 × 10−4 M. Aspirin produced a small, reproducible and statistically significant stimulation of the chromogenic activity of plasmin upon H-D-Valyl-L-Leucyl-L-Lysine-p-nitroanilide (3-2251) or pyro-Glu-Gly-Arg-p-nitroanilide (S-2444). Kinetic analysis demonstrated a slight decrease in the affinity of plasmin for substrate 3-2251 in the presence of aspirin, reflected by a change of the Km from 3.2 × 10-4 M to 3.8 × 10-4 M, and an increase of the Vm. The reciprocal Lineweaver-Burk curve indicated an uncompetitive type of stimulation. The stimulatory effect of aspirin was abolished by the lysine analogue α-aminohexanoic acid (AHA) but not by the α-amino acid glutamic acid. The effect of AHA suggests a specific involvement of lysine binding sites (LBS) on plasmin in the interaction of the enzyme with aspirin. Tlansient acidification of plasmin abolished its response to aspirin, to AHA and to their combination. The addition of aspirin to diluted human control or pregnancy plasma in vitro stimulated the plasma-mediated cleavage of the chromogenic substrate3-2251. In contrast to its effect on plasmin, aspirin failed to change the activity of tissue-type or urokinasetype plasminogen activators. It is conceivable that in addition to the antithrombotic effect of aspirin ascribed to its interaction with the platelets, aspirin also directly stimulates plasmin activity.