Why the study?
Does synthetic prostacyclin inhibit platelet retention and aggregation in whole blood passed through glass bead columns?
Does synthetic prostacyclin inhibit platelet retention and aggregation in whole blood passed through glass bead columns?
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Synthetic prostacyclin effectively inhibits platelet aggregation in a concentration-dependent manner but does not completely prevent initial platelet adhesion in an in vitro glass bead model.
As whole blood passes through a column of glass beads, platelets are activated and all 3 basic platelet properties (adhesion, release reaction and aggregation) displayed, an aspect similar to platelets being involved in a hemostatic process. For this reason, we chose the platelet retention test as the tool to study the effect of synthetic prostacyclin (PGI2) on platelet function and behavior. PGI2 inhibited platelet retention with its major impact on platelet aggregation. The extent of inhibition was not proportional to the concentration of PGI2. It appears that 2 levels of platelet aggregation take place inside the column. One, triggered by a weak stimulus, is readily inhibitable by low concentrations of PGI2. The other, brought about by a strong stimulus, requires higher concentrations of PGI2 to achieve complete inhibition. Even with as much as 100 ng PGI2/ml blood, a 15% retention remained which probably represented platelet adhesion to glass beads. Scanning electron microscopic examination of glass beads showed massive platelet aggregation and adhesion in control blood samples. No platelet aggregate was observed on beads filtered with blood containing 20 ng/ml or more PGI2. Individual platelets were found on glass beads filtered with samples containing any concentrations of PGI2; these platelets exhibited extensive morphologic changes.
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Ts'ao et al. (1982) studied this question.
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