Pulmonary microvascular endothelial cells are known to play an active role in the events that lead to vascular damage in the inflammatory response. The endothelial surface, normally immunologically privileged and very actively antithrombogenic, can respond to certain stimuli, generally injurious, by becoming strongly procoagulant and by expressing Fc and C3b receptors. Like macrophages, activated endothelial cells can provide a common source and substratum for combined hemostatic and complement-linked reactions. Such transformations of endothelial functions may involve alterations in the endothelial glycocalyx and, in addition, may be important for the entrapment and disposal of phagocytosed particulates. What is clear is that it is not simply absence of endothelium that has a bearing on the outcome of inflammatory stimuli but that structural and functional responses of the endothelial surface to injury, resulting in altered expression of hemostatic and immunologic potential, may have an important bearing on the role of the endothelium in the regulation of microvascular permeability.