Abstract
Heparin one unit/ml added in vitro to normal citrated PRP increases the platelet aggregation induced by ADP or Adrenaline with regard to aggregation measured in citrated PRP without heparin. This phenomenon is accompanied by an increase of the release reaction of 14C-5HT, ATP and ADP. In the same experimental conditions, pathological platelets (“aspirin-like syndrome”) respond by an increased aggregation without release reaction. This effect of heparin on normal or pathological platelet aggregation is inhibited by ASA or by Dipyridamole. – In citrated PRP obtained from blood of heparinized normal subjects, platelet aggregation and release reaction of platelets are increased with regard to their response tested before heparinization. Addition of ASA or Dipyridamole in PRP inhibits the effects of heparinization. – In two subjects with a platelet disease and a mild bleeding tendency, heparinization in vivo does not lengthen the bleeding time but increases the aggregation, without any release reaction. In vitro addition of ASA or Dipyridamole inhibits the increase of aggregation observed in absence of release reaction. -Besides their theoretical aspects concerning the mechanism of inhibition of platelet aggregation by ASA and Dipyridamole, these observations suggest the possible benefit of antiaggregant drugs for subjects treated by heparin.
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