Bureau M, Sourouille P, Brun-Pascaud M, Fey M, Pocidalo J J
Bull Eur Physiopathol Respir. 1985 Jul-Aug;21(4):325-9.
The vascular sequestration of polymorphonuclear leukocytes (PMN) may be responsible for endothelial injury leading to lung oedema, which occurs when rats are exposed to pure normobaric oxygen. Indeed, marginated PMN in close contact with the endothelium are able to damage the latter when activated. In the present work, marginated leukocytes were recovered by lavage through the pulmonary artery in isolated rat lung and the leukocyte differential count in blood and in the lung perfusion liquid (perfusate) was studied. Following 55 h of hyperoxia, a rise in the PMN count and lymphocytopenia were observed in the blood and in the perfusate. Moreover, the relatively greater increase in the PMN concentration in the perfusate than in the blood suggested a strengthening of their margination along the endothelium. A clear protective effect was noted during hyperoxia provided previous injection of endotoxin (1.5 mg X kg-1 intraperitoneally) had been performed. Indeed, after 65 h of hyperoxia, none of these rats (Endo/O2) died and there was no pleural effusion. The lymphocyte count was maintained within the normal limit and the number of PMN in the lung perfusion fluid and in blood was reduced. Results of this study suggest an essential role of the marginated PMN in lung oxygen toxicity.
多形核白细胞（PMN）的血管内扣押可能是导致内皮损伤进而引起肺水肿的原因，这种情况发生在大鼠暴露于纯常压氧时。实际上，与内皮紧密接触的边缘化PMN在被激活时能够损伤内皮。在本研究中，通过对离体大鼠肺脏进行肺动脉灌洗来回收边缘化白细胞，并研究血液和肺灌注液（灌流液）中的白细胞分类计数。高氧暴露55小时后，血液和灌流液中PMN计数升高且淋巴细胞减少。此外，灌流液中PMN浓度相对血液中的增加更大，这表明它们沿内皮的边缘化增强。如果事先进行内毒素注射（腹腔注射1.5 mg·kg-1），则在高氧暴露期间可观察到明显的保护作用。确实，高氧暴露65小时后，这些大鼠（内毒素/氧气组）均未死亡，也没有胸腔积液。淋巴细胞计数维持在正常范围内，肺灌注液和血液中的PMN数量减少。本研究结果表明边缘化PMN在肺氧中毒中起重要作用。
