Hainis K D, Sznajder J I, Schraufnagel D E
Section of Pulmonary and Critical Care Medicine, Michael Reese Hospital, Chicago, Illinois.
Am J Physiol. 1994 Aug;267(2 Pt 1):L199-205. doi: 10.1152/ajplung.1994.267.2.L199.
Lymphatics are important in the resolution of pulmonary edema, but which lymphatics drain alveolar fluid and how they change during lung injury and edema is uncertain. To study this question 16 rats were exposed to 85% O2 for 7 days. At 0, 3, 7, and 14 days after removal from the hyperoxic chamber, the lungs of the rats were cast by instilling methyl methacrylate into the trachea. The lungs of four similar room-air breathing rats served as controls. Tissue was taken for light microscopy and the casts were examined for lymphatic filling with a scanning electron microscope. Rats exposed to hyperoxia had diffuse damage and extensive edema. On removal from hyperoxia (day 0), 29% of the rat bronchioles had saccular lymphatic casts around them and 6% of bronchioles were surrounded by these lymphatics. Twenty-five percent of bronchioles had conduit lymphatic casts. Fourteen percent of arteries had lymphatic casts around them. All were different from the rats kept in room air (P < 0.0001). Rats exposed to hyperoxia had lymphatics on the pleural surface, near alveoli and alveolar ducts, and around veins. The peribronchial and periarterial saccular lymphatics formed separate groups with communicating conduit lymphatics. The perivenous lymphatics had their own separate conduit lymphatics. Fourteen days after returning to ambient air, the lymphatics were similar to those of control animals. In this model, airway casting allows three-dimensional analysis of the lung lymphatics. It shows that lymphatic compartments expand during hyperoxic lung injury and that peribronchial and perivascular saccular lymphatics connect to conduit lymphatics of the bronchoalveolar bundle.
淋巴管在肺水肿的消退过程中起着重要作用,但究竟哪些淋巴管引流肺泡液以及它们在肺损伤和水肿期间如何变化尚不清楚。为了研究这个问题,将16只大鼠暴露于85%的氧气中7天。在从高氧舱取出后的0、3、7和14天,通过向气管内注入甲基丙烯酸甲酯对大鼠的肺进行铸型。四只呼吸室内空气的类似大鼠的肺作为对照。取组织进行光学显微镜检查,并用扫描电子显微镜检查铸型的淋巴管充盈情况。暴露于高氧的大鼠有弥漫性损伤和广泛水肿。在从高氧环境中取出时(第0天),29%的大鼠细支气管周围有囊状淋巴管铸型,6%的细支气管被这些淋巴管包围。25%的细支气管有导管淋巴管铸型。14%的动脉周围有淋巴管铸型。所有这些都与饲养在室内空气中的大鼠不同(P < 0.0001)。暴露于高氧的大鼠在胸膜表面、肺泡和肺泡管附近以及静脉周围有淋巴管。支气管周围和动脉周围的囊状淋巴管与连通的导管淋巴管形成独立的组。静脉周围的淋巴管有其自己独立的导管淋巴管。回到常氧环境14天后,淋巴管与对照动物的相似。在这个模型中,气道铸型允许对肺淋巴管进行三维分析。结果表明,在高氧肺损伤期间淋巴管腔扩张,并且支气管周围和血管周围的囊状淋巴管与支气管肺泡束的导管淋巴管相连。