Gee M H, Perkowski S Z, Tahamont M V, Flynn J T
Fed Proc. 1985 Jan;44(1 Pt 1):46-52.
The pulmonary effects of intravascular complement activation can be divided into those that are initial events of activation and those that depend on the duration of intravascular activation. Pulmonary leukostasis is both an initial event and one that persists as long as intravascular complement activation is ongoing. This event is independent of synthesis and release of cyclooxygenase products of arachidonic acid. Initial events include synthesis and release of thromboxane and development of pulmonary hypertension and hypoxemia. Cyclooxygenase products are mediators of these initial pathophysiological events in part or in total. Complement-initiated increases in lung microvascular permeability are dependent on the duration of intravascular complement activation. Activation must be either prolonged or repeated to produce significant microvascular injury. This process is unrelated to synthesis and release of cyclooxygenase products, but is related to release of toxic oxygen metabolites.
血管内补体激活的肺部效应可分为激活的初始事件和取决于血管内激活持续时间的事件。肺白细胞淤滞既是初始事件，也是只要血管内补体激活持续就会持续存在的事件。该事件与花生四烯酸的环氧化酶产物的合成和释放无关。初始事件包括血栓素的合成和释放以及肺动脉高压和低氧血症的发生。环氧化酶产物部分或全部是这些初始病理生理事件的介质。补体引发的肺微血管通透性增加取决于血管内补体激活的持续时间。激活必须延长或重复才能产生显著的微血管损伤。这个过程与环氧化酶产物的合成和释放无关，但与有毒氧代谢产物的释放有关。
