1982年我们综述了成人呼吸窘迫综合征(ARDS)病因的当前概念。当时,循环血中白细胞(特别是粒细胞)的血管内活化作用正是令人兴趣盎然的一个课题。近来有一些报告说,观察到血透析引起中性白细胞减少,低氧血症,肺粒细胞隔绝,补体活化作用是这一现象的原因,而且补体活化作用预示病人ARDS的发作。这些报告暗示,对于ARDS病因有一个看法一致的假说,即补体活化作用使被激活的粒细胞粘附并损坏了肺微细血管的内皮细胞,结果是肺毛细血管渗透性增加,最后从肺泡溢出,导致呼吸衰竭。由于这一假说简单易明,故引人注意;又由于这一假说似能一举而阐明ARDS病因,鉴别出可能发生本综合征的病人,并提示可能的药物疗法,故令人振奋。对上述补体假说进一步支持的是利用支气 In 1982 we reviewed the current concept of the aetiology of adult respiratory distress syndrome (ARDS). At that time, the intravascular activation of circulating blood leukocytes, especially granulocytes, was an interesting topic. Recently there have been reports that hemodialysis was observed to cause neutropenia, hypoxemia, granulocyte isolation, and activation of complement, which are responsible for this phenomenon, and complement activation predicts the onset of ARDS in patients. These reports suggest that there is a consistent hypothesis regarding the etiology of ARDS that complement activation binds activated granulocytes and damages the pulmonary microvascular endothelial cells, resulting in increased pulmonary capillary permeability and eventually spillover from the alveoli, Resulting in respiratory failure. Because of the simplicity and clarity of the hypothesis, it is interesting to note that it is heartening to note that this hypothesis seems to shed some light on the etiology of ARDS, identify patients who may develop this syndrome and suggest possible drug regimens. Further support for the above complement hypothesis is the use of bronchi