“…The endothelial change involves, at a minimum, the expression of adhesion molecules that enable the monocytes to adhere to the vessel wall and undergo transendothelial migration in both large and small vessels, leading to local deposits of monocyte clusters in segments of the blood vessels. These monocyte clusters could then periodically signal the vessel endothelium via release of pro thrombotic, proinflammatory, and chemotactic me diators, such as TNF-a, IL-1, and perhaps platelet activating factor, to convert the endothelium to a procoagulant state and, in effect, prepare the vessel segments in a manner similar to the localized Shwartzman paradigm (Shwartzman, 1928;Movat , 1987;Hallenbeck et aI., 1988;Pober and Cotran, 1990). Complement activation or any stim ulus leading to activation of the coagulation system (including natural oscillation of coagulation poten tial, stress, infection, trauma, and inflammation) could then precipitate a localized reaction of the prepared vessel segment and lead to a local throm bosis or hemorrhage.…”