Increased sensitivity of arachidonic acid-induced platelet aggregation in the presence of carbon dioxide.
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.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology*; D002245:Carbon Dioxide / Q000494:pharmacology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007249:Inflammation / Q000097:blood; D010974:Platelet Aggregation / Q000187:drug effects*
D001095:Arachidonic Acids; D002245:Carbon Dioxide; D016718:Arachidonic Acid; D000244:Adenosine Diphosphate