1. A. Formation of the Platelet Plug
A. Formation of the Platelet Plug. Platelet plug formation results from the initial response of platelets to a site of blood vessel wall injury. Control of formation of the initial plug is via nitrous oxide and prostacyclins, as noted in the text. NO, nitric oxide. [Reproduced with permission from Kibble JD and Halsey CR: The Big Picture: Medical Physiology, 1st edition, McGraw-Hill, 2009.] B. Mechanism of Clot Formation by Platelets. Following the initial formation of a platelet plug, partly aided by exposed von Willebrand factor (vWF) at the injury site (see the figure), platelets continue to aggregate via fibrin linking of their Gp IIb/IIIa receptors. Adhesions by these receptors lead to activation of the platelets and degranulation, which releases adenosine diphosphate (ADP), thromboxane A2 (TXA2), and other factors, all of which further increase the formation of initial platelet plug/clot. As noted in Figure 14-14A, nitric oxide and antiplatelet prostacyclin (PGI2) limit plug and clot formation beyond the injury. The clotting cascade noted in the figure is described further below. EC, endothelial cell. [Reproduced with permission from Simmons ML and Decker JW: Br Heart J, McGraw-Hill, 1995.]
Source: Chapter 14. Blood, The Big Picture: Medical Biochemistry
Citation: Janson LW, Tischler ME. The Big Picture: Medical Biochemistry; 2012 Available at: Accessed: October 15, 2017
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