These studies of endothelial cell coagulant properties indicate the potentially active role of endothelium in the modulation of procoagulant and anticoagulant mechanisms. In addition, they draw attention to the different types of mechanisms that function in the maintenance of hemostasis and the induction of thrombosis. Hemostasis requires a rapid and complete response to injury in order to serve the host effectively; the optimal response to a penetrating injury involves rapid formation of a thrombus to prevent extravasation and maintain hemodynamics. In contrast, thrombosis could involve a more subtle and gradual modulation of cellular coagulant properties. An inflammatory mediator such as interleukin 1 could shift vessel wall coagulant properties over hours, and when coupled with an additional stimulus, such as perturbation of blood flow, could result in thrombus formation. The latter clot would form on a morphologically intact but functionally altered endothelium. Perturbation of endothelial cell coagulant properties by physiologic mediators of the host response may provide insights into mechanisms through which the vessel wall can contribute to the pathogenesis of thrombotic disease.