Key result
Addition of prostacyclin (PGI2) at 10(-7) M during isolation inhibited platelet activation, minimizing thromboxane production and beta-TG release compared to standard methods over 3 days of storage.
Why the study?
Does the addition of prostacyclin (PGI2) prevent platelet activation during the preparation of platelet concentrates?
Does the addition of prostacyclin (PGI2) prevent platelet activation during the preparation of platelet concentrates?
Adding prostacyclin during the preparation of platelet concentrates inhibits platelet activation, potentially improving the quality of stored platelets.
Answers are grounded in this paper and cite their sources.
PGI2 during isolation may preserve platelet quality in storage; leaves open clinical benefit in human transfusion.
Increased utilization of platelet concentrates (PCs) has created the possibility that demand for this blood component may exceed supply. It seems possible that this problem could be minimized if platelets could be isolated from whole blood and stored with full retention of hemostatic effectiveness. We prepared PCs by adding prostacyclin (PGI2) during the isolation procedure and compared these to PCs prepared without addition of PGI2. At concentration 10(-7) M, PGI2 inhibited activation of platelets during the process of concentration and resuspension by the criteria of minimal thromboxane production and release of beta thromboglobulin (beta-TG), in contrast to concentrates prepared by standard methods. These differences persisted throughout 3 days of storage at room temperature. Our findings suggest that further studies are indicated to determine whether the quality (hemostatic effectiveness) of concentrated platelets can be improved by pharmacologic means.
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Menitove et al. (1984) studied Platelet concentrate preparation. Prostacyclin (PGI2) vs. Standard methods (without addition of PGI2) was evaluated on Activation of platelets (thromboxane production and release of beta thromboglobulin). Addition of prostacyclin (PGI2) at 10(-7) M during isolation inhibited platelet activation, minimizing thromboxane production and beta-TG release compared to standard methods over 3 days of storage.
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