Decreased responsiveness and development of activation markers of PLTs stored in plasma

Circulating PLTs have a low activation state and high responsiveness, which ensures adequate hemostatic activity at sites of vessel wall damage. PLTs collected for transfusion purposes preferably have retained these properties to restore impaired hemostasis with thrombocytopenia.

We determined activation properties and coagulant activity of PLT-plasma preparations that were pooled or collected from single donors via apheresis.

In comparison to freshly isolated PLTs, both apheresis and pooled PLTs exhibited slow exposure of CD62 upon storage, followed by surface appearance of procoagulant phosphatidylserine (PS) but not activated integrin alpha IIb beta 3. During storage, thrombin- and ADP-induced Ca2+ signal generation consistently decreased in apheresis and pooled PLTs, which was accompanied by lower agonist-induced CD62 exposure and alpha IIb beta 3 activation. In flowing whole blood, stored apheresis PLTs showed lower collagen-induced Ca2+ responses and strikingly diminished participation in thrombus formation. Both apheresis and pooled PLT-plasma concentrates exhibited high tissue factor-triggered thrombin generation, which was insensitive to PLT inhibition and attributable to PS-exposing microparticles.

PLTs stored in plasma develop surface activation markers but, simultaneously, show markedly decreased responsiveness toward physiologic agonists. The plasma contains high coagulant activity, which is no longer PLT (activation)-dependent.