Solal-Celigny P, Meyohas M C
Rev Fr Mal Respir. 1983;11(5):751-67.
The activation, aggregation and adhesion of polymorphonuclear leukocytes on the endothelial wall of the pulmonary capillaries are responsible for lesions of variable severity on the alveolar-capillary membrane. The mechanism and the contribution of this leukocyte aggregation was studied to explain the respiratory abnormalities observed during the course of haemodialysis, leukapharesis and the end of extra-corporeal circulation. The activation of complement, by the formation of C5a is probably the initiator of this phenomenon. Based on these experimental models, the varied steps in the intra-capillary aggregation of leukocytes is envisaged as an explanation for the lesions in the acute respiratory distress syndrome, alveolitis caused by immune complexes and pulmonary toxicity caused by oxygen. Corticosteroids may inhibit leukocyte aggregation under certain conditions. These studies allow for a more precise pathophysiological approach for the use of steroids in their disorders.
多形核白细胞在肺毛细血管内皮壁上的激活、聚集和黏附是造成肺泡-毛细血管膜不同程度损伤的原因。为了解释血液透析、白细胞去除术及体外循环末期观察到的呼吸异常情况，对这种白细胞聚集的机制及作用进行了研究。补体通过形成C5a而激活，可能是这一现象的起始因素。基于这些实验模型，白细胞在毛细血管内聚集的不同步骤被设想为对急性呼吸窘迫综合征、免疫复合物引起的肺泡炎及氧引起的肺毒性中损伤情况的一种解释。在某些情况下，皮质类固醇可能会抑制白细胞聚集。这些研究为在疾病中使用类固醇提供了更精确的病理生理学方法。
