Idell S
Pulmonary Division, University of Texas Health Center at Tyler.
New Horiz. 1994 Nov;2(4):566-74.
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.
血管外纤维蛋白沉积是急性炎症反应的特征，例如，在成人呼吸窘迫综合征患者的肺泡腔中很明显。损伤肺组织中的纤维蛋白沉积受局部表达的凝血途径和纤维蛋白清除途径（称为纤维蛋白溶解）平衡的调节。这些途径是影响局部炎症细胞运输、微血管通透性和修复机制的相互作用反应网络的一部分。从这个意义上说，肺内纤维蛋白周转超出了传统的止血范畴，可能影响急性炎症反应及其消退。在受损的肺泡腔内，纤维蛋白沉积由与因子VII相关的外源性凝血途径——组织因子的活性增加引发。接触和内源性凝血途径也会激活。局部纤维蛋白溶解通常受损，这可能会增强血管外纤维蛋白沉积。成年哺乳动物肺内的纤维蛋白周转在几种损伤形式中同样受到破坏，但与患有呼吸窘迫的早产儿肺损伤不同。
