Lucht W D, English D K, Bernard G R, Serafin W E, Brigham K L
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee.
Am J Med Sci. 1987 Sep;294(3):161-7. doi: 10.1097/00000441-198709000-00006.
Interactions of granulocytes with the lungs are altered by endotoxemia and may be critical in the pathogenesis of endotoxin-induced lung injury. In chronically instrumented unanesthetized sheep, we measured the ability of lung lymph to aggregate normal sheep neutrophils in vitro. We found a marked increase in lung lymph aggregating activity beginning within 1 hour after endotoxin infusion and persisting for several hours. When n-acetylcysteine was administered to the animals before endotoxin infusion, neutrophil aggregating activity in lung lymph after endotoxin infusion was markedly reduced. N-acetylcysteine did not affect neutrophil aggregation, adherence, or leukotriene B4 production in vitro and did not prevent complement activation at concentrations achieved in vivo. It is concluded that endotoxemia causes release from the lungs of substance(s) that activate granulocytes, and that this response is prevented by n-acetylcysteine, possibly as a result of the antioxidant properties of the drug.
内毒素血症会改变粒细胞与肺的相互作用，这可能在内毒素诱导的肺损伤发病机制中起关键作用。在长期植入仪器的未麻醉绵羊中，我们测量了肺淋巴液在体外聚集正常绵羊中性粒细胞的能力。我们发现，内毒素输注后1小时内肺淋巴液聚集活性显著增加，并持续数小时。在内毒素输注前给动物施用N-乙酰半胱氨酸，内毒素输注后肺淋巴液中的中性粒细胞聚集活性显著降低。N-乙酰半胱氨酸在体外不影响中性粒细胞聚集、黏附或白三烯B4的产生，且在体内达到的浓度下不会阻止补体激活。结论是，内毒素血症导致肺释放激活粒细胞的物质，而这种反应可被N-乙酰半胱氨酸阻止，这可能是由于该药物的抗氧化特性所致。
