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Platelet Hyperaggregability, Blood Prostacyclin and Dipyridamole

From the Department of Physiology, U.L.B. Free Univerity of Brussels, Brussels, Belgium

M. Kahn

From the Department of Physiology, U.L.B. Free Univerity of Brussels, Brussels, Belgium

M. Cloarec

From the Hospital Tenon Polyclinic, C.H.U. Saint-Antoine, University of Paris VI, Paris, France

J. Van De Merckt

From the Department of Radiotherapy-Onocology, Saint-Luc University Clinic, Catholic University of Louvain, Louvain, Belgium

R. Sneppe

Department of Audiophonology, Catholic University of Louvain, Louvain, Belgium

E. Schram

the Institute for Molecular Biology, V.U.B., Free University of Brussels, Brussels, Belgium

J.V. Fenollar

From the Department of Cardiology and Oncology, Valencia University, Valencia, Spain

This study demonstrates the presence of PGI₂ in blood and its influence on platelet retention tests, possibly by the intermediate of a releasing system in the columns, which is followed by a proximate recuperation on the erythrocyte sites after the passage.

The presence of prostacyclin on the erythrocyte sites seems to depend upon the red cell deformability in relation to the good condition of their erythrycote ATP reserve.

The load of the erythrocyte sites increases with the daily dose of dipyrida mole. The maximum load of the sites appears to be reached with a daily dose of dipyridamole 450mg.

Approximately 10% of the atherosclerosis patients who have been treated by dipyridamole keep their platelet hyperaggregability and their abnormally low ered prostacyclin level.

Angiology, Vol. 37, No. 3, 175-184 (1986)
DOI: 10.1177/000331978603700306


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