Kerry P J, Paton C J
Br J Pharmacol. 1984 Jan;81(1):125-30. doi: 10.1111/j.1476-5381.1984.tb10752.x.
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.
作为模拟炎症和组织液淤积中观察到的pH值和PCO₂变化的一种手段,已对二氧化碳对枸橼酸化的人富血小板血浆(PRP)的影响进行了研究。在经二氧化碳处理的PRP中,二磷酸腺苷(ADP)诱导的血小板聚集受到抑制。相比之下,经二氧化碳处理的血小板对花生四烯酸钠的敏感性提高了八倍,并且在添加花生四烯酸钠前1分钟添加外源性钙可模拟这种效应。如果让二氧化碳从经处理的PRP中扩散,随后将其暴露于空气中,二氧化碳对ADP诱导的和花生四烯酸钠诱导的聚集的影响就会消除,这表明血小板代谢没有永久性改变。随着pH值降低,花生四烯酸钠诱导的聚集敏感性增加可能是影响止血过程中血小板行为的一个重要因素。