Shennib H, Mulder D S, Chiu R C
Arch Surg. 1984 Mar;119(3):274-7. doi: 10.1001/archsurg.1984.01390150016004.
Pulmonary atelectasis predisposes the lung to infection. This condition may be partly due to impaired cellular immune response of the collapsed lung segment. We postulated that atelectasis may affect alveolar macrophage (AM) antibacterial function. To test this hypothesis, atelectasis was induced in the right upper lobes of piglet lungs. Alveolar macrophages harvested by bronchoalveolar lavage of collapsed segments for up to 24 hours showed progressive depression of their phagocytic activity against Pseudomonas aeruginosa in vitro. However, their intracellular bactericidal activity did not change. Reexpansion of the atelectatic lobes with mechanical ventilation and 100% oxygen supplementation for four hours after six hours of atelectasis resulted in reversal of the impaired AM phagocytic activity. These observations presented insight into the mechanisms of susceptibility to lung infection in pulmonary atelectasis and the potential for its reversal.
肺不张使肺部易于感染。这种情况可能部分归因于萎陷肺段的细胞免疫反应受损。我们推测肺不张可能会影响肺泡巨噬细胞（AM）的抗菌功能。为了验证这一假设，在仔猪肺的右上叶诱导形成肺不张。通过对萎陷肺段进行支气管肺泡灌洗采集的肺泡巨噬细胞，在长达24小时的时间里，其对铜绿假单胞菌的体外吞噬活性呈进行性降低。然而，它们的细胞内杀菌活性并未改变。在肺不张6小时后，通过机械通气和补充100%氧气对萎陷肺叶进行复张4小时，导致受损的肺泡巨噬细胞吞噬活性得到逆转。这些观察结果为肺不张时肺部感染易感性的机制及其逆转潜力提供了见解。
