Abstract
Heparin at concentrations used clinically inhibits the anti-aggregating effect of prostacyclin (PGI 2) and prostaglandin D 2 (PGD 2). Inhibition is dose-dependent and is related to the concentration of the prostaglandin. Aggregation induced by ADP, epinephrine, arachidonate, and the ionophore A23187 is not inhibited by concentrations of PGI 2 which prevent aggregation in the absence of heparin. Doubling the PGI 2 concentration overcomes the heparin antagonism, while further raising the heparin dose restores the antagonism of PGI 2 activity. Heparin acts immediately, and is effective even if added after platelet exposure to PGI 2. Dextran sulfate, but not neutral dextrans, have similar action. Both heparin and dextran sulfate reverse the platelet inhibitory effect of supernatant fluids from stimulated endothelial cell monolayers which contain PGI 2. It is possible that some of the unusual adverse effects of heparin therapy may in part relate to the heparin antagonism of vascular PGI 2.
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