Laboratory investigation of platelet function: a review of methodology.

Yardumian, D. A.; Mackie, Ian; Machin, S.J.

doi:10.1136/jcp.39.7.701

Cited by 93 publications

(44 citation statements)

References 33 publications

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“…Clearly the platelet content of aequorin was not exhausted by stimulation with collagen and that after the onset of aggregation, Ca2+ was removed from the cytoplasm by its resequestration on the reticular membranes. As has been reported by others, collagen-induced aggregation was preceded by a lag phase of approximately 30s [24], but both collagen and A231 87 caused an almost instantaneous rise in [Ca2+Ii which may reflect modulation of platelet aggregation to collagen by a post-receptor mediated mechanism independent of the mobilization of Ca2+.…”

Section: Methodssupporting

confidence: 72%

Platelet transmembrane signalling responses to collagen in familial hypercholesterolaemia

Cooper

Tan

Betteridge

1994

Eur J Clin Investigation

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Abstract.Washed platelets from patients with familial hypercholesterolaemia (FH) were found to be more reactive towards collagen than those from control subjects. The dose required to achieve half maximum aggregation was found to be 0.6 ml-' for FH patients whilst that for control subjects was 1.25 pg ml-'. In both types of platelet, intracellular Ca2+ levels, as monitored by the Ca2+-dependent photoprotein, aequorin, rose on stimulation with collagen and then fell to basal levels, probably due to resequestration by the reticular system. This effect was not due to exhaustion of the supply of aequorin since sustained Ca2+ influx induced by the ionophore, A23 187, gave a stable signal that did not return to baseline. Similarly, inositol 1,4,5, trisphosphate levels increased in the cytosol after stimulation and then fell to unstimulated values. When stimulated with collagen, platelets from FH patients showed a greater extent of cytoplasmic calcium mobilization ( P < 0-05) when compared to controls, coupled with a greater extent of inositol phospholipid hydrolysis ( P < 0.05). At doses of collagen sufficient to give either 100% or 50% aggregation, platelets from patients or control subjects showed the same amplitude of ATP release at either dose suggesting that the trigger for vesicle release is more sensitive in FH.

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Section: Methodssupporting

confidence: 72%

Platelet transmembrane signalling responses to collagen in familial hypercholesterolaemia

Cooper

Tan

Betteridge

1994

Eur J Clin Investigation

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“…Since its first description in 1962 by Born, platelet aggregometry has become the most widely used laboratory method to screen patients for inherited or acquired defects of platelet function [1,2]. Optical aggregometry measures the increase in light transmission through platelet-rich plasma that occurs when platelets are aggregated by adding an agonist.…”

Section: Introductionmentioning

confidence: 99%

Standardization of light transmittance aggregometry for monitoring antiplatelet therapy: an adjustment for platelet count is not necessary

Linnemann

Schwonberg

Mani

et al. 2008

Journal of Thrombosis and Haemostasis

129

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To cite this article: Linnemann B, Schwonberg J, Mani H, Prochnow S, Lindhoff-Last E. Standardization of light transmittance aggregometry for monitoring antiplatelet therapy: an adjustment for platelet count is not necessary. J Thromb Haemost 2008; 6: 677-83.Summary. Background: Light transmittance aggregometry (LTA) is considered to be the Ôgold standardÕ of platelet function testing. As LTA has been poorly standardized, we analyzed the results of LTA in healthy subjects and patients with antiplatelet therapy using different concentrations of agonists and performing tests in non-adjusted and platelet count-adjusted platelet-rich plasma (PRP). Methods: LTA was performed in 20 healthy subjects and in patients treated with aspirin (n = 30) or clopidogrel (n = 30) monotherapy, as well as in patients on combination therapy (n = 20), using arachidonic acid (ARA 0.25 and 0.5 mg mL ) and adenosine diphosphate (ADP 2 and 5 lM) as agonists and performing platelet function tests in non-adjusted and platelet count (250 nL )1 ± 10%)-adjusted PRP. Results: The overall platelet aggregation response is decreased after adjusting the PRP for platelet count compared with measurements in unadjusted PRP. The variability of aggregation results is high in adjusted PRP in the subgroup of healthy subjects, ranging from 9.2-95.3% (5th-95th percentile) relative to 77.6-95.5% in nonadjusted PRP when determining maximum aggregation to ARA 0.5 mg mL )1. Late aggregation using ADP 2 lM ranges from 3.8-89.9% in adjusted PRP compared with 42.9-92.5% in non-adjusted PRP. Maximum aggregation using ARA 0.5 mg mL )1 in non-adjusted PRP differentiates between aspirin-treated patients and healthy controls well, whereas late aggregation using ADP 2 lM in non-adjusted PRP offers the best discrimination between clopidogrel-treated patients and healthy controls. Conclusion: Adjustment of PRP for platelet count does not provide any advantage and therefore the time-consuming process of platelet count adjustment is not necessary.

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“…61 All of these mechanisms share a final common pathway dependent on the surface glycoprotein IIb/IIIa complex (GP IIb/IIIa). Fibrinogen is the ligand for the GP IIb/IIIa receptor and is responsible for amplification of the aggregation response.…”

Section: Gp Iib/iiia Receptor Antagonistsmentioning

confidence: 99%

Antiplatelet Therapy in Acute Cerebral Ischemia

Bednar

Gross

1999

Stroke

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Background-Improved recognition of stroke signs and symptoms has paralleled the development of pharmacological strategies that may be examined to reduce stroke mortality and morbidity. Presently, tissue plasminogen activator is the only therapy that significantly improves outcome in acute stroke, with no agent demonstrating a significant reduction in mortality. Summary of Review-Antiplatelet agents are a heterogenous class of drugs that have been successfully used for more than 2 decades in secondary stroke prevention. These agents include aspirin, with or without dipyridamole, and more recently, the adenosine antagonists ticlopidine and clopidogrel. However, studies of the use of antiplatelet agents within 48 hours of the ictus have examined only aspirin. Only 1 study, the Multicentre Acute Stroke Trial-Italy (MAST-I), entered patients within 6 hours of the ictus. These data suggest that an improvement in mortality may be related to the speed of administration. No significant adverse events were noted with early antiplatelet monotherapy. However, MAST-I did note a significant increase in early mortality in patients receiving aspirin plus streptokinase, a finding not adequately explained by an increase in the intracranial hemorrhage rate. Conclusions-The use of antiplatelet therapy in acute stroke, clinical or experimental, has only recently received attention.It is likely that the use of antiplatelet agents for acute stroke therapy will be less restrictive than that currently seen for thrombolytics. Future studies should include an examination of those agents that have previously demonstrated efficacy in secondary stroke prevention, most notably, aspirin. The recognition that all platelet stimuli share a final common pathway that is dependent on the surface glycoprotein IIb/IIIa (fibrinogen) receptor has resulted in the development of various agents which block this receptor and are currently the focus for clinical trials. The role of nitric oxide in stroke therapy will depend on minimizing the hypotensive side effects of this agent. Stroke models are needed to provide preliminary data on the efficacy of antiplatelet therapy, especially as relates to the interaction of antiplatelet agents with thrombolytics. (Stroke. 1999;30:887-893.)

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Laboratory investigation of platelet function: a review of methodology.

Cited by 93 publications

References 33 publications

Platelet transmembrane signalling responses to collagen in familial hypercholesterolaemia

Platelet transmembrane signalling responses to collagen in familial hypercholesterolaemia

Standardization of light transmittance aggregometry for monitoring antiplatelet therapy: an adjustment for platelet count is not necessary

Antiplatelet Therapy in Acute Cerebral Ischemia

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