Storage of platelets for tests of platelet function: Effects of pH on platelet aggregation and liberation of β-thromboglobulin

Ketanserin is a well-known serotonin S₂ receptor antagonist but its capacity to inhibit serotonin-induced aggregation ex vivo during chronic administration has been a matter of debate. In vitro evidence is presented that the inhibitory capacity of ketanserin is lowered by increasing plasma pH. Since the pH of plasma kept at the open air increases with time, we studied the effect of chronic administered ketanserin on serotonin-induced platelet aggregation in plasma kept at a lowered pH of 7.70, by replacing the air with 95% O₂–5% CO₂. Using this slightly modified technique, we could, in contrast to our previous studies, observe a complete inhibition of the serotonin-induced aggregation throughout the ketanserin treatment period.

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“…As seen with other agonists [5,[7][8][9][10], this aggregation is very much dependent on pH conditions [ 11].…”

Section: Discussionmentioning

confidence: 99%

Continuous Inhibition of Serotonin-Induced Platelet Aggregation during Chronic Ketanserin Administration to Man Can Be Detected after Plasma pH Control

Arnout¹,

Russelt²,

Deckmyn³

et al. 1987

Pathophysiol Haemos Thromb

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“…However, it is unclear whether basic platelet functions such as adhesion, aggregation or granule secretion are affected by these pathological changes in extracellular pH. Early studies that aimed to optimise aggregation techniques suggest that platelet aggregation is inhibited by acidosis as a result of decreased calcium mobilisation (6)(7)(8)(9), and a widely used protocol for preparation of washed platelets includes the adjustment of pH at 6.5 (7). To date, most studies investigating the effect of pH on platelet physiology focus on optimising the conditions for the platelet aggregation techniques, or on application of freeze-drying techniques for blood bank storage.…”

Section: Introductionmentioning

confidence: 99%

Acidosis downregulates platelet haemostatic functions and promotes neutrophil proinflammatory responses mediated by platelets

Etulain

Negrotto²,

Carestia³

et al. 2012

Thromb Haemost

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Acidosis is one of the hallmarks of tissue injury such as trauma, infection, inflammation, and tumour growth. Although platelets participate in the pathophysiology of all these processes, the impact of acidosis on platelet biology has not been studied outside of the quality control of laboratory aggregation assays or platelet transfusion optimization. Herein, we evaluate the effect of physiologically relevant changes in extracellular acidosis on the biological function of platelets, placing particular emphasis on haemostatic and secretory functions. Platelet haemostatic responses such as adhesion, spreading, activation of αIIbβ3 integrin, ATP release, aggregation, thromboxane B2 generation, clot retraction and procoagulant activity including phosphatidilserine exposure and microparticle formation, showed a statistically significant inhibition of thrombin-induced changes at pH of 7.0 and 6.5 compared to the physiological pH (7.4). The release of alpha granule content was differentially regulated by acidosis. At low pH, thrombin or collagen-induced secretion of vascular endothelial growth factor and endostatin were dramatically reduced. The release of von Willebrand factor and stromal derived factor-1α followed a similar, albeit less dramatic pattern. In contrast, the induction of CD40L was not changed by low pH, and P-selectin exposure was significantly increased. While the generation of mixed platelet-leukocyte aggregates and the increased chemotaxis of neutrophils mediated by platelets were further augmented under acidic conditions in a P-selectin dependent manner, the increased neutrophil survival was independent of P-selectin expression. In conclusion, our results indicate that extracellular acidosis downregulates most of the haemostatic platelet functions, and promotes those involved in amplifying the neutrophil-mediated inflammatory response.

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“…17 We have data which show that platelet injury induced by storage conditions is associated with the release of f3TG from platelets in PRP. 6 The data from the present study show that when platelets were stored as whole blood there was less f3TG liberation than from platelets stored as platelet concentrates. Although this may indicate less injury, these results may only reflect the differences in storage temperature, since there is known to be less liberation of f3TG at 4 QC than at room temperature.…”

Section: Discussionmentioning

confidence: 43%

Platelet Function in Platelet Concentrates and in Whole Blood

Rodgers

Lloyd

Russell

1985

Anaesth Intensive Care

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Platelet function was studied in CPD whole blood stored at 4QC for one and three days and in platelet concentrates stored at room temperature for the same periods of time. Comparisons were made of platelet shape, nucleotide content, (3-thromboglobulin ((3TO) liberated during storage, and platelet aggregation in response to ADP, collagen, sodium arachidonate and ristocetin. It was found that in whole blood the shape of the platelets was less discoid than in platelet concentrates. However, platelet aggregation in response to ADP, collagen, and sodium arachidonate was preserved better in whole blood than in platelet concentrates. Platelet nucleotides were the same in whole blood as in platelet concentrates, but the plasma levels of (3 TO were less in whole blood. The results show that as judged by aggregation, (3 TO release and nucleotide content, platelets from whole blood were at least as functional as those from platelet concentrates. However, platelets from whole blood had lost their discoid shape, which suggests that they would have a short survival in the circulation.

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Storage of platelets for tests of platelet function: Effects of pH on platelet aggregation and liberation of β-thromboglobulin

Cited by 32 publications

References 7 publications

Continuous Inhibition of Serotonin-Induced Platelet Aggregation during Chronic Ketanserin Administration to Man Can Be Detected after Plasma pH Control

Continuous Inhibition of Serotonin-Induced Platelet Aggregation during Chronic Ketanserin Administration to Man Can Be Detected after Plasma pH Control

Acidosis downregulates platelet haemostatic functions and promotes neutrophil proinflammatory responses mediated by platelets

Platelet Function in Platelet Concentrates and in Whole Blood

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