Unindicted Coconspirators in Inflammatory Tissue Injury
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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, PGF2α), the endoperoxides (eg, PGH2), and thromboxane A2 (TxA2). TxA2 and, to a lesser extent, PGF2α 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 …