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目的：探讨肺脏在老龄大鼠多器官衰竭中的作用。方法：一次性静脉主射大肠杆菌内毒素，复制出老龄大鼠多器官衰竭（ＭＯＦ）实验模型。动态观察了五个时相组（１、２、６、１２、２４ｈ）的有关免疫、生化功能指标和病理变化。结果：内毒素注射后１～２ｈ，肺脏首先发生衰竭，表现为呼吸窘迫，动脉血氧分压（ＰａＯ２）下降、肺泡气与动脉血氧分压差（Ａ－ａＤＯ２）增高、血清ＡＣＥ活性降低、Ｃ５ａ增高。肺组织的ＴＮＦ、ＳＯＤ、ＬＰＯ显著增高。病理示：肺泡膈水肿增厚，肺间质和肺泡出血，水肿及大量炎细胞浸润、积聚。而此时相其它器官均无功能指标和病理异常变化。６ｈ后大鼠均发生ＭＯＦ。结论：（１）肺脏是老龄大鼠ＭＯＦ的首发器官；（２）肺衰竭后低氧血症和肺内产生大量炎性介质在老龄大鼠ＭＯＦ发生发展中起到了促发作用
Objective: To investigate the role of lung in multiple organ failure in aging rats. Methods: One-time intravenous injection of endotoxin of Escherichia coli to replicate the experimental model of multiple organ failure (MOF) in aged rats. Dynamic observation of the five phase group (1,2,6,12,24 h) on immune, biochemical function and pathological changes. Results: After 1 ~ 2h injection of endotoxin, the lungs first developed failure, manifested as respiratory distress, decreased arterial oxygen pressure (PaO2), increased alveolar gas and arterial oxygen difference (A-aDO2), and decreased serum ACE activity , C5a increased. Lung tissue TNF, SOD, LPO was significantly higher. Pathology: thickening of the alveolar septum, pulmonary interstitial and alveolar hemorrhage, edema and a large number of inflammatory cell infiltration, accumulation. Other organs at this time no other functional indicators and pathological changes. After 6h, rats developed MOF. Conclusions: (1) The lungs are the first organs of MOF in aged rats; (2) hypoxemia after pulmonary failure and massive inflammatory mediators in the lungs play a role in the development of MOF in the aged rats