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Abstract
Furosemide in vitro is an inhibitor of primary ADP-induced platelet aggregation. As
such, furosemide also inhibits collagen-induced aggregation and the secondary wave
of epinephrine-induced aggregation. Concentrations of furosemide which clearly inhibit
collagen-induced platelet aggregation do not inhibit collagen-induced release of ADP.
Thus the effect of furosemide is distinct from that of aspirin and other anti-inflammatory
drugs which inhibit platelet release but do not inhibit primary ADP-induced platelet
aggregation. The inhibitory effect of furosemide is competitive, demonstrable in heparinized
as well as citrated platelet-rich plasma, and it is not corrected by calcium. The
concentration of furosemide required for in vitro inhibition (1 to 5mM) can not be
achieved in vivo. However, the study of compounds related to furosemide could lead
to the discovery of a clinically useful inhibitor of primary ADP-induced platelet
aggregation.
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Article info
Publication history
Accepted:
September 29,
1972
Received:
March 28,
1972
Footnotes
☆This work was supported by the Paul V. Galvin Charitable Trust.
Identification
Copyright
© 1973 Published by Elsevier Inc.