The comparative ability of platelets isolated from blood samples stabilized with sodium citrate, edta, or heparin to aggregate in response to activation by certain agonists

The ability to activate platelets isolated from blood samples stabilized with sodium citrate, EDTA or heparin and located in plasma containing the same anticoagulant was studied. Platelets found in plasma were induced to activate in vitro by adding agents such as epinephrine, thrombin, or thrombin+thromboxane-A2. The ability of platelets to form aggregates, which were microscopically visualized in phase contrast, was used as an activation marker. The studies showed that platelets isolated from blood samples stabilized with any of the abovementioned anticoagulants did not aggregate in response to the addition of adrenaline. Platelets isolated from blood stabilized with sodium citrate and EDTA retained the ability to aggregate after plasma recalcification, but did not aggregate in response to the addition of thrombin. However, platelets isolated from sodium citrate-stabilized blood, unlike platelets isolated from EDTA-stabilized blood, aggregated in response to the addition of thrombin along with thromboxane-A2. Platelets isolated from heparin-stabilized blood were moderately aggregated for thrombin activation and very strongly for thrombin + thromboxane-A2 activation. The results of the study obtained in an in vitro model indicate that platelets isolated from blood samples stabilized with sodium citrate or EDTA, after their introduction into the patient's tissues as part of plasma containing the same anticoagulant, will be able to activate and realize their regenerative potential only under the condition of rapid recalcification. And platelets obtained in the form of plasma enriched with platelets from heparinstabilized blood samples will be able to activate and realize their regenerative potential only if the injected anticoagulant does not interfere with the processes of plasma and platelet hemostasis at the injection site and, accordingly, the synthesis of thrombin and thromboxane-A2.