Closa D, Sabater L, Fernández-Cruz L, Prats N, Gelpí E, Roselló-Catafau J
Department of Medical Bioanalysis, Institut d'Investigaciones Biomediques August P. Sunyer, Institut d'Investigaciones Biomediques de Barcelona--Consejo Superior de Investigaciones Cientificas, Spain.
Ann Surg. 1999 Feb;229(2):230-6. doi: 10.1097/00000658-199902000-00011.
To evaluate (1) whether alveolar macrophages are activated as a consequence of acute pancreatitis (AP), (2) the implication of inflammatory factors released by these macrophages in the process of neutrophil migration into the lungs observed in lung injury induced by AP, and (3) the role of the liver in the activation of alveolar macrophages.
Acute lung injury is the extrapancreatic complication most frequently associated with death and complications in severe AP. Neutrophil infiltration into the lungs seems to be related to the release of systemic and local mediators. The liver and alveolar macrophages are sources of mediators that have been suggested to participate in the lung damage associated with AP.
Pancreatitis was induced in rats by intraductal administration of 5% sodium taurocholate. The inflammatory process in the lung and the activation of alveolar macrophages were investigated in animals with and without portocaval shunting 3 hours after AP induction. Alveolar macrophages were obtained by bronchoalveolar lavage. The generation of nitric oxide, leukotriene B4, tumor necrosis factor-alpha, and MIP-2 by alveolar macrophages and the chemotactic activity of supernatants of cultured macrophages were evaluated.
Pancreatitis was associated with increased infiltration of neutrophils into the lungs 3 hours after induction. This effect was prevented by the portocaval shunt. Alveolar macrophages obtained after induction of pancreatitis generated increased levels of nitric oxide, tumor necrosis factor-alpha, and MIP-2, but not leukotriene B4. In addition, supernatants of these macrophages exhibited a chemotactic activity for neutrophils when instilled into the lungs of unmanipulated animals. All these effects were abolished when portocaval shunting was carried out before induction of pancreatitis.
Lung damage induced by experimental AP is associated with alveolar macrophage activation. The liver mediates the alveolar macrophage activation in this experimental model.
评估（1）肺泡巨噬细胞是否因急性胰腺炎（AP）而被激活；（2）这些巨噬细胞释放的炎性因子在AP诱导的肺损伤中观察到的中性粒细胞向肺部迁移过程中的作用；（3）肝脏在肺泡巨噬细胞激活中的作用。
急性肺损伤是严重AP中最常与死亡和并发症相关的胰腺外并发症。中性粒细胞浸润到肺部似乎与全身和局部介质的释放有关。肝脏和肺泡巨噬细胞是已被认为参与与AP相关的肺损伤的介质来源。
通过导管内注射5%牛磺胆酸钠诱导大鼠胰腺炎。在诱导AP 3小时后，对有和没有门腔分流的动物进行肺部炎症过程和肺泡巨噬细胞激活的研究。通过支气管肺泡灌洗获得肺泡巨噬细胞。评估肺泡巨噬细胞产生一氧化氮、白三烯B4、肿瘤坏死因子-α和MIP-2的情况以及培养巨噬细胞上清液的趋化活性。
胰腺炎诱导3小时后，与中性粒细胞向肺部的浸润增加有关。门腔分流可预防这种效应。诱导胰腺炎后获得的肺泡巨噬细胞产生的一氧化氮、肿瘤坏死因子-α和MIP-2水平增加，但白三烯B4没有增加。此外，当将这些巨噬细胞的上清液注入未处理动物的肺部时，它们对中性粒细胞表现出趋化活性。在诱导胰腺炎前进行门腔分流时，所有这些效应均被消除。
实验性AP诱导的肺损伤与肺泡巨噬细胞激活有关。在这个实验模型中，肝脏介导肺泡巨噬细胞的激活。
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