Article date: January 1984
By: P. J. Kerry, Catherine J. Paton in Volume 81, Issue 1, pages 125-130
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.
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.
DOI: 10.1111/j.1476-5381.1984.tb10752.x
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