[Complement, granulocytes and pulmonary capillaries].

P Solal-Celigny, M C Meyohas
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Abstract

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.

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补体、粒细胞和肺毛细血管。
多形核白细胞在肺毛细血管内皮壁上的激活、聚集和粘附是肺泡毛细血管膜不同程度病变的原因。研究了这种白细胞聚集的机制和作用,以解释在血液透析、白细胞流失和体外循环结束过程中观察到的呼吸异常。补体的活化,通过C5a的形成可能是这一现象的始作俑者。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急性呼吸窘迫综合征、免疫复合物引起的肺泡炎和氧引起的肺毒性病变的解释。在某些条件下,皮质类固醇可抑制白细胞聚集。这些研究为在其疾病中使用类固醇提供了更精确的病理生理学方法。
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