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Effects of heparin on platelet aggregation and release and thromboxane A2 production

Journal Article · · Am. J. Pathol.; (United States)
OSTI ID:5589402

Heparin, when added to citrated platelet-rich plasma (PRP), caused potentiation of platelet aggregation and the release reaction induced by the aggregating agents adenosine diphosphate (ADP), arachidonic acid, collagen, and epinephrine. At low concentrations (4.7 x 10(-5) M) arachidonic acid failed to cause aggregation of platelets in citrated PRP. However, in the presence of heparin, the same concentration of arachidonic acid caused aggregation. Examination of PRP for the presence of thromboxane A2 (TxA2) by use of a bioassay revealed that heparin also stimulated release of TxA2. This finding indicated that platelets released more TxA2 when they were challenged by low concentrations of arachidonic acid in the presence of heparin than in its absence. Platelets were labeled with /sup 3/H-arachidonic acid and /sup 14/C-serotonin, and attempts were made to determine whether heparin stimulated the platelet release reaction first with subsequent increased production of TxA2, or alternatively, whether heparin stimulated TxA2 production first with subsequent enhancement of the release reaction. In view of the demonstrated simultaneous release of /sup 14/C-serotonin and /sup 3/H-arachidonic acid metabolites, it appeared that either release of /sup 14/C and /sup 3/H occurs concurrently or, even if one of these events is dependent on the other, both events take place in rapid succession. Timed sequential studies revealed that in the presence of arachidonic acid, the addition of heparin hastened the apparently simultaneous release of both /sup 14/C and /sup 3/H.

OSTI ID:
5589402
Journal Information:
Am. J. Pathol.; (United States), Journal Name: Am. J. Pathol.; (United States) Vol. 104:2; ISSN AJPAA
Country of Publication:
United States
Language:
English