Extravascular coagulation and fibrin deposition in acute lung injury

Abstract

Extravascular fibrin deposition is characteristic of the acute inflammatory response and is, for example, prominent in the alveolar compartment of patients with the adult respiratory distress syndrome. Fibrin deposition in the injured lung is regulated by a balance of locally expressed pathways of coagulation and fibrin clearance, called fibrinolysis. These pathways comprise part of the interactive network of responses that influence local inflammatory cell traffic, microvascular permeability, and repair mechanisms. In this sense, fibrin turnover in the lung extends beyond traditional hemostasis and may influence the acute inflammatory response and resolution. Within the injured alveolar compartment, fibrin deposition is initiated by increased activity of the extrinsic coagulation pathway-tissue factor associated with factor VII. Activation of the contact and intrinsic coagulation pathways also occurs. Local fibrinolysis is generally impaired, which may potentiate extravascular fibrin deposition. Fibrin turnover in the adult mammalian lung is similarly disrupted in several forms of injury but differs from the injury that occurs in the lungs of premature infants with respiratory distress.