Platelets have recently been shown to participate in reactions with blood coagulation factors at every stage of intrinsic clotting, from contact activation to fibrin formation. Platelets can trigger intrinsic coagulation by two alternative pathways, the first of which involves factors XII and XI and adenosine diphosphate, and the second of which bypasses factor XII, provided factor XI and collagen are present. Additional evidence indicates that subsequent coagulation reactions occur on the platelet surface, where active clotting factors are protected from inactivation by naturally occurring inhibitors. Based on these observations, an hypothesis is presented in which the events of primary hemostasis (platelet adhesion, aggregation, and release) and blood coagulation are linked. As platelets aggregate to form a hemostatic plug, they provide a protective and catalytic surface for activation of the clotting mechanism and fibrin formation. Localized hemostasis is promoted and circulating blood kept fluid by means of a number of control mechanisms, some of which are mediated by autocatalytic effects of thrombin.

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