Key result
Small citrate increments markedly inhibit platelet aggregation induced by ADP, epinephrine, and collagen.
Why the study?
The impact of citrate concentration on platelet aggregation induced by various agonists and its implications for clinical platelet aggregation studies and antiplatelet drug assessment was unclear.
Does increased citrate concentration affect human platelet aggregation induced by various agents?
Does increased citrate concentration affect human platelet aggregation induced by various agents?
Controlling the citrate:blood ratio is critical in clinical platelet aggregation studies and antiplatelet drug assessment, as excess citrate markedly inhibits aggregation.
Answers are grounded in this paper and cite their sources.
Citrate concentration must be tightly controlled in platelet testing; leaves open standardization needs for reliable clinical and research use.
The effects of citrate concentration on adenosinediphosphate-, epinephrine-, collagen-, and ristocetin-induced human platelet aggregation were investigated. Relatively small increments in citrate concentration markedly inhibited platelet aggregation by all three physiologic agents. The inhibitory effect was greatest on epinephrine-induced aggregation, and least on collagen-induced aggregation. Ristocetin-induced aggregation was not affected by excess citrate anticoagulation. These findings indicate the importance of controlling the citrate:blood ratio in clinical platelet aggregation studies and in the assessment of antiplatelet drugs.
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Ts'ao et al. (1976) studied Human platelet aggregation. Citrate concentration was evaluated on Platelet aggregation induced by adenosinediphosphate, epinephrine, collagen, and ristocetin. Relatively small increments in citrate concentration markedly inhibited platelet aggregation induced by adenosinediphosphate, epinephrine, and collagen, but not ristocetin.
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