ABSTRACT
This chapter reviews studies that aid in elucidating the coordinant mechanisms by which fibrinolysins remove fibrinous deposits and modulate fibrin-related tissue remodeling within the lung. The lung would seem to be particularly susceptible to derangements in coagulation and fibrinolysis. It functions to expose the entire cardiac output to environmental air by virtue of an enormous network of micrometer-thick membranes organized into millions of air sacs with a total surface area of nearly 70 m. Evolution of the molecular definition of lung fibrinolysins has paralleled the ascent in understanding of tissue fibrinolysins in general. The expression and regulation of urokinase receptor in human lung cells other than macrophages is much less well defined, although the early work of M. B. Bernik and H. C. Kwaan implies their presence, as has subsequent work with isolated alveolar epithelial cells and interstitial fibroblasts. Fluid-phase fibrinolytic activity is depressed in both acute and chronic inflammatory lung disease.
