Helset E, Ytrehus K, Tveita T, Kjaeve J, Jørgensen L
Department of Anaesthesiology, University of Tromsø, Norway.
Circ Shock. 1994 Dec;44(4):201-9.
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.
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有白细胞。本研究检测了大鼠静脉注射ET-1是否会在肺中引发炎症反应。ET-1输注2小时后对肺标本进行组织学检查，结果显示肺血管中的白细胞黏附于血管内皮，且肺毛细血管中有白细胞滞留。对支气管肺泡灌洗液进行显微镜检查发现白细胞已迁移至肺泡。同时观察到外周血白细胞减少。这些效应在24小时后可逆转。对全身血流动力学效应的监测显示，2小时后心搏量持续降低，心率增加。在离体大鼠肺中，ET-1可使肺动脉压、肺微血管压迅速升高，并导致肺水肿形成。与用 Krebs-白蛋白灌注的肺相比，血液灌注加速了ET-1的致水肿效应。ET-1在肺循环中白细胞与内皮细胞相互作用的调节中发挥作用。这对于ET-1的致水肿效应具有潜在重要意义。
