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4 - Platelet heterogeneity: physiology and pathological consequences

from PART I - PHYSIOLOGY

Published online by Cambridge University Press:  10 May 2010

Anthony Mathur
Affiliation:
Centre for Cardiovascular Biology and Medicine, University College London, UK
John F. Martin
Affiliation:
Centre for Cardiovascular Biology and Medicine, University College London, UK
Paolo Gresele
Affiliation:
Università degli Studi di Perugia, Italy
Clive P. Page
Affiliation:
Sackler Institute of Pulmonary Pharmacology and Therapeutics, Guy's, King's and St Thomas' School of Biomedical Sciences, London
Valentin Fuster
Affiliation:
Mount Sinai Medical Center and School of Medicine, New York
Jos Vermylen
Affiliation:
Universiteitsbibliotheek-K.U., Leuven
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Summary

Introduction

Individual platelets vary in terms of volume, density and reactivity. Ever since the seminal paper by Karpatkin, the biological significance of this platelet heterogeneity has been strongly contested.

Platelet volume, usually measured as mean platelet volume (MPV), has been the most frequently studied platelet physical variable. During steady-state hematopoeisis the platelet volume distribution approaches log normality with platelets ranging in size from <2 µm3 to >15 µm3 in volume. This variation in size is considerably greater than that observed for other circulating blood elements in any mammal. This heterogeneity forms the basis of the controversy with respect to the physiological relevance of platelet volume and reactivity.

Separation of platelets into size dependent subpopulations has shown that the granular contents of these cells is directly proportional to their volume. Importantly, the ability of platelets to affect each other and their environment as measured by aggregation and total amount of granular contents released, is proportional to their size and confirmed by the finding that platelet volume correlates with absolute platelet function. The physiological explanation for this lies in the observation that high-density platelets contain significantly higher concentrations of alpha granule proteins (β thromboglobulin, von Willebrand factor), dense granule markers (5-HT, calcium), mitochondrial marker enzymes (monamine oxidase, cytochrome oxidase, glutamate dehydrogenase and NADP-dependent isocitrate dehydrogenase), glycogen and express more of the GPIIb/IIIa receptor.

Type
Chapter
Information
Platelets in Thrombotic and Non-Thrombotic Disorders
Pathophysiology, Pharmacology and Therapeutics
, pp. 70 - 79
Publisher: Cambridge University Press
Print publication year: 2002

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