内皮素-1引起肺循环中白细胞的积累。

Circulatory shock Pub Date : 1994-12-01
E Helset, K Ytrehus, T Tveita, J Kjaeve, L Jørgensen
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引用次数: 0

摘要

我们之前报道过内皮素-1 (ET-1)诱导的离体大鼠肺微血管通透性增加需要灌注液中的白细胞。本研究探讨了大鼠静脉注射ET-1是否会引起肺部炎症反应。ET-1输注2小时后肺标本的组织学检查显示,肺血管内白细胞粘附于血管内皮,白细胞在肺毛细血管内被隔离。支气管肺泡灌洗液镜检显示白细胞已迁移到肺泡内。同时观察到外周血白细胞的减少。这些影响在24小时内可逆。监测全身血流动力学效应显示,2小时后心脏搏量持续减少,心率增加。在离体大鼠肺中,ET-1引起肺动脉压、肺微血管压和水肿形成的快速升高。与krebs -白蛋白灌注肺相比,血液灌注加速ET-1的消肿作用。ET-1在肺循环中调节白细胞与内皮细胞的相互作用。这对ET-1的减脂作用具有潜在的重要性。
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Endothelin-1 causes accumulation of leukocytes in the pulmonary circulation.

We previously reported that the endothelin-1 (ET-1)-induced increase in microvascular permeability in isolated rat lungs required leukocytes in the perfusate. The present study examines whether intravenous administration of ET-1 in rats causes an inflammatory reaction in the lungs. Histological examination of the lung specimens 2 hr following ET-1 infusion showed adhesion of leukocytes to the vascular endothelium in pulmonary vessels and sequestration of leukocytes in the pulmonary capillaries. Microscopic examination of the bronchoalveolar lavage fluid revealed that leukocytes had migrated into the alveoli. Simultaneously a depletion of peripheral blood leukocytes was observed. These effects were reversible by 24 hr. Monitoring of systemic hemodynamic effects showed a continued reduced cardiac stroke volume and increasing heart rate after 2 hr. In isolated rat lungs, ET-1 caused a rapid increase in pulmonary artery pressure, pulmonary microvascular pressure, and edema formation. Compared with Krebs-albumin-perfused lungs, blood-perfusion accelerated the edemagenic effect of ET-1. ET-1 plays a role in the regulation of leukocyte-endothelial cell interactions in the pulmonary circulation. This has potential importance for the edemagenic effect of ET-1.

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