Why the study?
Does the addition of PGI2 reverse spontaneous platelet aggregation in vitro in whole blood from healthy young males?
Does the addition of PGI2 reverse spontaneous platelet aggregation in vitro in whole blood from healthy young males?
Prostacyclin-sensitive platelet aggregates in the blood of young volunteers appear to form in vitro rather than in vivo, as the de-aggregatory effect of prostacyclin is absent immediately after blood collection but enhanced by storage.
Answers are grounded in this paper and cite their sources.
PGI2 de-aggregation in stored blood may reflect in vitro artifact; leaves open in vivo relevance of platelet micro-aggregates in healthy subjects.
When unstirred citrated blood of young males was left to stand at 21 degrees C, the number of free platelets decreased as measured with a whole blood platelet counter. This decrease indicated spontaneous platelet aggregation (SPA) since it was accompanied by the time-dependent increase in platelet micro-aggregates and plasma beta-thromboglobulin while lactate dehydrogenase level did not change significantly. Addition of PGI2 to whole blood increased free platelet count and decreased the number of platelet micro-aggregates. The de-aggregatory effect of PGI2 (measured as a percentage increase in free platelet number) was correlated with the initial amount of platelet micro-aggregates. Blood storage enhanced SPA and de-aggregatory effect of prostacyclin. Immediately after blood collection de-aggregatory effect of prostacyclin was absent. Our results favour an assumption that prostacyclin-sensitive platelet aggregates in blood of young volunteers are formed in vitro rather than in vivo.
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Spławińska et al. (1987) studied this question.
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