December 1, 1986Biochemical JournalOpen Access

Platelet-activating factor (PAF-acether) induces high- and low-affinity binding of fibrinogen to human platelets via independent mechanisms

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Population

Human platelets

Comparison

Incubation with 500 nM-PAF-acether vs Preincubation with inhibitors of…

Design

Preclinical

Authors

EKE KloproggeUniversity of Groningen JAJ W N AkkermanUtrecht University

Discussion

Member takes

Implication

Highlights dual PAF-induced platelet fibrinogen-binding pathways; leaves open whether selective inhibition improves antithrombotic efficacy.

Structured PICO

Population

Human platelets

Intervention

Incubation with 500 nM-PAF-acether (platelet-activating factor)

Comparator

Preincubation with inhibitors of cyclo-oxygenase (acetylsalicylic acid, indomethacin), thromboxane synthetase (UK 38.485), or ADP scavengers

Outcome

Exposure of high- and low-affinity fibrinogen binding sitessurrogate

PAF-acether induces high- and low-affinity fibrinogen binding to human platelets via independent mechanisms involving thromboxane A2 and secreted ADP.

Cite This Study

Kloprogge et al. (1986) studied this question.

synapsesocial.com/papers/6a87dab49f534feb2aad262b https://doi.org/10.1042/bj2400403

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Implication

Highlights dual PAF-induced platelet fibrinogen-binding pathways; leaves open whether selective inhibition improves antithrombotic efficacy.

Platelet-activating factor (PAF-acether) induces high- and low-affinity binding of fibrinogen to human platelets via independent mechanisms

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Platelet-activating factor (PAF-acether) induces high- and low-affinity binding of fibrinogen to human platelets via independent mechanisms

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider