Modulation of Platelet-neutrophil Interaction with Pharmacological Inhibition of Fibrinogen Binding to Platelet GPIIb/IIIa Receptor

Zihui Xiao; Pierre Théroux; Mony Frojmovic

doi:10.1055/s-0037-1614458

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1999; 81(02): 281-285
DOI: 10.1055/s-0037-1614458

Review Articles

Schattauer GmbH

Modulation of Platelet-neutrophil Interaction with Pharmacological Inhibition of Fibrinogen Binding to Platelet GPIIb/IIIa Receptor

Zihui Xiao

¹From the Department of Medicine, Montreal Heart Institute, Montreal, Quebec, Canada

,

Pierre Théroux

²The Department of Medicine, University of Montreal, Montreal, Quebec, Canada

,

Mony Frojmovic

³Department of Physiology, McGill University, Montreal, Quebec, Canada

› Author Affiliations

Abstract

Summary

The study investigated how drug inhibition of the GPIIb/IIIa receptor influences the interactions between platelets and leukocytes. These interactions are believed to play an important role in the etiology of the acute coronary syndromes. Thirty patients with unstable angina or non-Q-wave myocardial infarction were studied before the administration of tirofiban or placebo and after 4 h and 72 h. Platelet-leukocyte aggregates were characterized in whole blood using three-colour flow cytometry. The leukocyte population was isolated by a nucleic acid probe (LDS 751) and platelet-neutrophil coaggregates identified as particles binding both anti-CD42a-FITC and anti-CD45-PE. Tirofiban decreased by 25% the density of platelets in circulating platelet-neutrophil coaggregates (p <0.01), and prevented the increase induced by platelet agonist stimulation (p <0.0001). The reduction correlated with inhibition of fibrinogen binding to platelet (p <0.0001) and with inhibition of platelet aggregation (p <0.0001). The percentage of neutrophils with bound platelets following platelet agonist stimulation was, however, increased following GPIIb/IIIa inhibition. Thus, inhibition of GPIIb/IIIa receptor promotes platelet-neutrophil adhesion, but markedly reduces the binding density of platelets in the coaggregates.

Full Text

References

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