地塞米松对内毒素豚鼠肺白细胞血容量和白蛋白运动的干扰

C.M.M.B. de Castro , M.F. Bureau, B.B. Vargaftig, M. Bachelet
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引用次数: 1

摘要

使用放射性示踪剂,我们测量了静脉注射脂多糖(0.1 - 1mglkg)后肺内的血容量、白蛋白交换和血白细胞隔离。在平行实验中观察中性粒细胞对气道的浸润情况。地塞米松预处理(20mg /kg,皮下)不能预防脂多糖引起的早期肺改变,如血容量减少、白细胞隔离、白细胞减少或跨内皮白蛋白交换增加。然而,在脂多糖处理的豚鼠中观察到,地塞米松对后期白蛋白通过内皮/上皮屏障渗漏和气道中性粒细胞积累提供了显著的保护。我们的研究结果表明,地塞米松对脂多糖诱导的肺损伤的保护作用可能源于最初白细胞粘附的减少和后来肺泡毛细血管通透性的降低。
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Interference of dexamethasone with leukocyte blood volume and albumin movements in lungs from endotoxemic guinea-pigs

Using radioactive tracers, we measured blood volume, albumin exchanges and blood leukocyte sequestration within lungs, following an intravenous injection of lipopolysaccharide (0.1–1 mglkg). Neutrophil infiltration into the airways was followed in parallel experiments. Dexamethasone pretreatment (20 mg/kg, subcutaneous) failed to prevent early pulmonary changes induced by lipopolysaccharide as decreased blood volume, leukocyte sequestration, leukopenia or the increased trans-endothelial albumin exchanges. However, dexamethasone provided a significant protection against the later albumin leakage through the endothelial/epithelial barrier and the neutrophil accumulation in the airways observed in lipopolysaccharide-treated guinea-pigs. Our results indicate that the protective effect of dexamethasone in lipopolysaccharide-induced lung injury might derive from an initial reduction of leukocyte adhesion and a later decrease in alveolo-capillary permeability.

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