Abstract

The effects of carbon dioxide on citrated human platelet-rich plasma (PRP) have been studied as a means of imitating the changes in pH and PCO2 observed in inflammation and tissue fluid stasis. Adenosine diphosphate (ADP)-induced platelet aggregation was inhibited in CO2-treated PRP. In contrast, CO2-treated platelets were rendered up to eight times more sensitive to sodium arachidonate and this effect could be imitated by the addition of exogenous calcium 1 min before the addition of arachidonate. The effects of CO2 on ADP-induced and arachidonate-induced aggregation were abolished if the CO2 was allowed to disperse from treated PRP subsequently exposed to air, suggesting no permanent alteration in platelet metabolism. The increased sensitivity of arachidonate-induced aggregation with lowered pH may be a significant factor in influencing platelet behaviour in haemostasis.

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