Borges J, Sckell A, Kübler W M, Goetz A E, Messmer K
Institut für Chirurgische Forschung, Klinikum Grosshadern, Ludwig-Maximilians-Universität München.
Langenbecks Arch Chir Suppl Kongressbd. 1998;115(Suppl I):709-11.
In the pulmonary circulation, endotoxemia induces leukocyte/endothelium interaction in pulmonary arterioles and venules. Thus, leukocytes may contribute to the pathogenesis of acute lung injury. In order to investigate, whether this interaction can be inhibited by early blockade of the adhesion cascade, we studied the effect of the humanized anti-L-selectin antibody HuDreg 200 on leukocyte kinetics in pulmonary arterioles and venules following i.v.-infusion of endotoxin. In endotoxemia HuDreg 200 reduces sticking of leukocytes in both pulmonary arterioles and venules. Thus, we were able to demonstrate that early blockade of the adhesion cascade effectively prevents leukocyte accumulation in pulmonary microvessels in endotoxemia. Therefore, HuDreg 200 may exhibit protective effects on the manifestation of leukocyte-mediated acute lung injury.
在肺循环中,内毒素血症可诱导肺小动脉和小静脉中的白细胞/内皮细胞相互作用。因此,白细胞可能参与急性肺损伤的发病机制。为了研究这种相互作用是否能通过早期阻断黏附级联反应来抑制,我们研究了人源化抗L-选择素抗体HuDreg 200对静脉注射内毒素后肺小动脉和小静脉中白细胞动力学的影响。在内毒素血症中,HuDreg 200可减少白细胞在肺小动脉和小静脉中的黏附。因此,我们能够证明早期阻断黏附级联反应可有效防止内毒素血症时肺微血管中白细胞的积聚。因此,HuDreg 200可能对白细胞介导的急性肺损伤表现出保护作用。