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(Circulation Research. 2000;87:1077.)
© 2000 American Heart Association, Inc.

Editorial

Platelets

Unindicted Coconspirators in Inflammatory Tissue Injury

Allan M. Lefer

From the Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pa.

Correspondence to Allan M. Lefer, Department of Physiology, Jefferson Medical College, Thomas Jefferson University, 1020 Locust St, Philadelphia, PA 19107-6799. E-mail Allan.M.Lefer@mail.tju.edu

Key Words: platelets • leukocytes • endothelium • inflammation

	Introduction

 
In the 1970s, during the peak of eicosanoid research, platelets were generally considered to play a major role in mediating the cell and tissue injury known to occur in cerebral ischemia/stroke, myocardial ischemia/infarction, and traumatic injury to other organs or regions. Foremost among the platelet-derived humoral mediators of this type of tissue injury were the prostaglandins (eg, PGF₂), the endoperoxides (eg, PGH₂), and thromboxane A₂ (TxA₂). TxA₂ and, to a lesser extent, PGF₂ and PGH₂ are potent vasoconstrictors and thus can reduce blood flow to vital vascular beds.^{1 2} Moreover, these agents are also prothrombotic by virtue of potently stimulating platelet aggregation.^{1 2} These two effects can, of course, work together to constrict and obstruct microvessels. In fact, a popular and useful research protocol of that era was the intravenous injection of arachidonic acid, the precursor of the eicosanoids, into rabbits, resulting in a severe pulmonary thrombosis/vasoconstriction and sudden cardiopulmonary death.³ Because platelets are the primary source of TxA₂, release of TxA₂ aggregates other platelets and stimulates their release of additional TxA₂, thus propagating this response. Platelets also release serotonin, ADP, and catecholamines, which are contained within storage granules. These platelet-propagated processes are all considered to be major factors contributing to direct ischemic injury as occurs in myocardial and cerebral ischemia. With the discovery of the mechanism of action of aspirin,^{4 5} this area of pathophysiology was addressed in a very practical way. Presently, aspirin is widely used in transient ischemic attacks, which often are precursors of strokes, . . . [Full Text of this Article]

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