Malik A B, Horgan M J
Am Rev Respir Dis. 1987 Aug;136(2):467-70. doi: 10.1164/ajrccm/136.2.467.
We have examined the mechanisms of lung vascular injury and pulmonary edema secondary to intravascular coagulation. Alpha-thrombin was infused intravenously to induce pulmonary intravascular coagulation. The results indicate that fibrin and neutrophils are essential requirements for lung vascular injury and pulmonary edema formation. The findings point to a fibrin-neutrophil interaction in inducing neutrophil adherence. Thrombin also has direct effects on endothelial permeability and can contribute to neutrophil sequestration in the lung by increasing endothelial adhesivity. Complement activation can explain only a part of the response. Lipid-derived mediators (e.g., LTB4 and mono HETEs) may be particularly important in the pathophysiology of lung vascular injury and pulmonary edema.
我们研究了血管内凝血继发的肺血管损伤和肺水肿的机制。静脉注射α-凝血酶以诱导肺血管内凝血。结果表明，纤维蛋白和中性粒细胞是肺血管损伤和肺水肿形成的必要条件。这些发现表明在诱导中性粒细胞黏附中存在纤维蛋白-中性粒细胞相互作用。凝血酶对内皮通透性也有直接作用，并且可通过增加内皮黏附性导致中性粒细胞在肺内滞留。补体激活只能解释部分反应。脂质衍生介质（如白三烯B4和单羟基二十碳四烯酸）在肺血管损伤和肺水肿的病理生理学中可能特别重要。
