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1 - History of platelets
- from PART I - PHYSIOLOGY
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- By J. Fraser Mustard, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada; Present address: The Founders' Network-CIAR, 401 Richmond St., Suite 281, Toronto, Ontario, Canada M5V 3A8, Raelene L. Kinlough-Rathbone, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada, Marian A. Packham, Department of Biochemistry, University of Toronto, Toronto, Ontario, Canada
- Edited by Paolo Gresele, Università degli Studi di Perugia, Italy, Clive P. Page, Valentin Fuster, Jos Vermylen, Universiteitsbibliotheek-K.U., Leuven
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- Book:
- Platelets in Thrombotic and Non-Thrombotic Disorders
- Published online:
- 10 May 2010
- Print publication:
- 30 May 2002, pp 3-24
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Summary
Introduction
In this chapter, we have concentrated on early observations that helped to open up new avenues of research, brought about greater understanding of hemorrhagic and arterial thromboembolic disorders, and in some instances led to new diagnostic methods and novel treatments for the complications of atherosclerosis. Over the years, technological developments have provided more and more tools for investigation. In the 1950s, electron microscopy began to reveal the fine structure of platelets, platelet aggregates, and thrombi. In the 1960s, aggregometers stimulated experiments with aggregating agents and their inhibitors; now, the pace has quickened with the introduction of flow cytometry, molecular biology techniques, monoclonal antibodies, genetically engineered animals and other new approaches.
Findings from research in other fields have frequently been applied to platelets, and knowledge about platelet functions has increased exponentially in the last 50 years. Time and time again, several groups almost simultaneously reported similar new results, but seldom has the rivalry been acrimonious. Some of the key players in the years between 1950 and 1980 have retired or are no longer with us, but this brief history mentions a few of the many contributions they made when the field was young.
Since other chapters will deal with recent findings, we have not attempted to provide a detailed history of the many new topics under investigation, such as the signalling pathways in platelets.
23 - Aggregation
- from PART I - PHYSIOLOGY
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- By Marian A. Packham, Department of Biochemistry, University of Toronto, Ontario, Canada, Margaret L. Rand, Division of Hematology/Oncology, The Hospital for Sick Children, Toronto, Ontario, Canada, Raelene L. Kinlough-Rathbone, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
- Edited by Paolo Gresele, Università degli Studi di Perugia, Italy, Clive P. Page, Valentin Fuster, Jos Vermylen, Universiteitsbibliotheek-K.U., Leuven
-
- Book:
- Platelets in Thrombotic and Non-Thrombotic Disorders
- Published online:
- 10 May 2010
- Print publication:
- 30 May 2002, pp 338-356
-
- Chapter
- Export citation
-
Summary
Introduction
Platelet aggregation is involved in the formation of hemostatic plugs and arterial thrombi. Under normal circumstances, platelets are non-adhesive and circulate singly, but following vessel wall injury they adhere to the injury site and to each other. During the hemostatic process, platelet aggregates, stabilized by fibrin, arrest bleeding from injured or severed vessels. In contrast to this useful function, platelet aggregates that form on injured vessels, on ruptured atherosclerotic plaques, or in regions of high shear contribute to the narrowing of blood vessels. If thrombi are unstable, they may embolize and block smaller vessels downstream from an injury site. Since platelet aggregation has a major role in the clinical complications of atherosclerosis (myocardial infarction, ischemic stroke, and peripheral vascular disease), there is intensive study of the processes involved in platelet aggregation and of inhibitors of platelet activation.
In vivo, activators of platelets include the agonists that are listed in Table 23.1. Receptors for some of the most important agonists are discussed in Chapters 8–11. Aggregating agents can act singly, and are frequently studied singly in vitro, but in vivo they undoubtedly act in concert with each other in a process described as synergism. Synergistic responses result in a combined effect that is greater than the additive effects of the single stimuli. In vivo, the most important aggregating agents are collagen in the vessel wall, ADP from red blood cells or released from the platelets themselves, thromboxane A2 formed by stimulated platelets, and thrombin, although other agonists such as serotonin may contribute to the aggregation process.