Key result
In vitro exposure to as little as 10 pg/ml of prostacyclin significantly reduced platelet aggregation in response to adenosine diphosphate and collagen.
Why the study?
Do low concentrations of prostacyclin reduce platelet aggregation in vitro in venous blood from healthy volunteers?
Do low concentrations of prostacyclin reduce platelet aggregation in vitro in venous blood from healthy volunteers?
Low concentrations of prostacyclin, similar to systemic spillover during inhaled therapy, cause a marked platelet aggregation defect in vitro that is not detected by TEG.
Answers are grounded in this paper and cite their sources.
Low prostacyclin inhibits platelet aggregation in vitro undetected by TEG; leaves open bleeding risk during inhaled therapy.
The study was performed to determine the possible direct effects of low concentrations of prostacyclin that might spill over into the systemic circulation during the administration of inhaled aerosolized prostacyclin. Platelet aggregation in response to adenosine diphosphate and collagen, as well as measurement of the maximum amplitude of the thrombelastograph (TEG), was undertaken in vitro using venous blood exposed to low concentrations of prostacyclin (0, 10, 100 and 500 pg/ml) from eight healthy volunteers. There were statistically significant reductions in parameters of platelet aggregation in response to the agonists adenosine diphosphate (1 mumol/l and 8 mumol/l) and collagen (10 mumol/l) following exposure to as little as 10 pg/ml of prostacyclin. The maximum amplitude of the TEG was unchanged over the entire range of prostacyclin concentrations studied. The results indicate that low concentrations of prostacyclin or prostacyclin metabolite such as may be observed during inhaled aerosolized prostacyclin therapy are likely to be associated with a marked platelet aggregation defect. This defect was not detected by the TEG.
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Heerden et al. (1997) studied Healthy volunteers (n=8). Prostacyclin vs. 0 pg/ml was evaluated on Platelet aggregation in response to adenosine diphosphate and collagen, and maximum amplitude of the thrombelastograph (TEG). In vitro exposure to as little as 10 pg/ml of prostacyclin significantly reduced platelet aggregation in response to adenosine diphosphate and collagen.
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