Heparin Counteracts the Antiaggregating Effect of Prostacyclin by Potentiating Platelet Aggregation

Abstract

SummaryIt has recently been reported that heparin neutralizes the inhibitory effect of prostacyclin (PGI2) on human platelet aggregation. The mechanism of this interaction has not yet been unequivocally established. We present here evidence that heparin (Liquemin Roche) does not react directly with PGI2 but counteracts its inhibitory effect by potentiating platelet aggregation. In the absence of heparin, PGI2 was a less effective inhibitor of platelet aggregation induced by the combination of ADP and serotonin than by ADP alone. Moreover, the inhibitory effect of PGI2 was similarly reduced when increasing the concentrations of ADP (in the absence of heparin). The lack of a specific interaction between heparin and PGI2 is supported by the observation that, in the presence of heparin, other prostaglandins such as PGD2 and PGE1, and a non-prostanoid compound such as adenosine also appeared to lose their inhibitory potency. It is concluded that heparin opposes platelet aggregation inhibitory effect of PGI2 by enhancement of platelet aggregation.

Interaction of a new low molecular weight heparin (OP/LMWH) with human platelets

“…In PGI2 interaction studies we observed that in PAF and ADP-induced platelet aggregation H counteracted the inhibiting activity of prostacyclin, as reported in the literature [9]. Furthermore OP/LMWH slightly affected the inhibition produced by PGI2…”

“…It has also been reported that conventional heparin counteracts platelet antiaggregating effect of prostacyclin [8,9] but no information is available about LMWH.…”

Maintaining blood flow in the extracorporeal circuit: haemostasis and anticoagulation

“…PGI2 is generally used with heparin for anticoagulation of ECCs although heparin interferes with the inhibitory effect of PGI2 on platelet aggregation in vitro [22,51]. A dose of 2.5-10 ng/kg/min often allows heparin dosages to be reduced to a minimum [52] or in some cases can completely replace heparin [53].…”

Interaction Between Glycosaminoglycans, Platelets, and Leukocytes

“…However, it has been questioned whether anticoagulation is fully re sponsible for the antithrombotic activity of heparin. [1][2][3] Heparin has been reported to influence platelet function, either by reducing [4][5][6] or enhancing platelet aggrega tion, [7][8][9][10][11][12] and to increase the number of fibrinogen recep tors on the platelet surface. 13 About 5% of patients re ceiving heparin develop thrombocytopenia.…”