静脉注射抗 MHC 类 I（H-2K）单克隆抗体后小鼠肺水潴留的活体观察。
Intra-vital Observation of Lung Water Retention Following Intravenous Injection of Anti-MHC-class I (H-2K) Monoclonal Antibody in Mice.
机构信息
Department of Perioperative Medicine, Division of Anesthesiology, Showa University, School of Dentistry, Tokyo, Japan.
Department of Perioperative Medicine, Division of Anesthesiology, Showa University, School of Dentistry, Tokyo, Japan
出版信息
In Vivo. 2019 Sep-Oct;33(5):1477-1484. doi: 10.21873/invivo.11627.
BACKGROUND/AIM: Leukocyte activation is thought to be a major step in sepsis-induced pulmonary edema. We attempted to confirm whether pulmonary edema can be reproduced under intravital microscopy in a model of transfusion-related acute lung injury (TRALI) using MHC class I-specific antibody.
MATERIALS AND METHODS
The surface pulmonary microcirculation was observed using an epi-fluorescence microscope through a thoracic window in 50 male mice. Monoclonal MHC class I-specific antibody (Ab) was administered to the animals, while the control group received saline. The leukocytes and macro-molecular leakage in the pulmonary circulation were analyzed.
RESULTS
Leukocytes accumulated in the capillaries (52.5±12.7 leukocytes per designated area in Ab group vs. 20.8±3.1 in control). The air-containing alveolus area significantly shrank from 2,224.9±934.9 μm to 509.7±380.8 μm in the Ab group.
CONCLUSION
Pulmonary edema develops rapidly following leukocyte accumulation in the lung. We confirmed that leukocyte accumulation without an underlining condition is sufficient to induce pulmonary edema.
背景/目的：白细胞激活被认为是脓毒症引起肺水肿的主要步骤。我们试图通过 MHC Ⅰ类特异性抗体，在输血相关急性肺损伤（TRALI）模型中，通过活体显微镜来确认是否可以重现肺水肿。
材料和方法
通过胸腔窗在 50 只雄性小鼠中的荧光显微镜观察肺表面微循环。向动物给予单克隆 MHC Ⅰ类特异性抗体（Ab），而对照组则给予生理盐水。分析肺循环中的白细胞和大分子渗漏。
结果
白细胞在毛细血管中积聚（Ab 组中每指定区域有 52.5±12.7 个白细胞，而对照组为 20.8±3.1）。Ab 组的含气肺泡面积从 2224.9±934.9μm显著缩小到 509.7±380.8μm。
结论
在肺中白细胞积聚后，肺水肿迅速发展。我们证实，没有潜在条件的白细胞积聚足以诱导肺水肿。
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