Hideyuki Ochi1, Takehiko Iijima2, Akira Ushiyama3. 1. Department of Perioperative Medicine, Division of Anesthesiology, Showa University, School of Dentistry, Tokyo, Japan. 2. Department of Perioperative Medicine, Division of Anesthesiology, Showa University, School of Dentistry, Tokyo, Japan iijima@dent.showa-u.ac.jp. 3. Department of Environmental Health, National Institute of Public Health, Saitama, Japan.
Abstract
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 μm2 to 509.7±380.8 μm2 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. Copyright
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 μm2 to 509.7±380.8 μm2 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. Copyright
Authors: Michaël Chassé; Lauralyn McIntyre; Shane W English; Alan Tinmouth; Greg Knoll; Dianna Wolfe; Kumanan Wilson; Nadine Shehata; Alan Forster; Carl van Walraven; Dean A Fergusson Journal: Transfus Med Rev Date: 2016-02-09
Authors: Mark R Looney; Xiao Su; Jessica A Van Ziffle; Clifford A Lowell; Michael A Matthay Journal: J Clin Invest Date: 2006-05-18 Impact factor: 14.808
Authors: Mark R Looney; John X Nguyen; Yongmei Hu; Jessica A Van Ziffle; Clifford A Lowell; Michael A Matthay Journal: J Clin Invest Date: 2009-10-05 Impact factor: 14.808
Authors: John W Semple; Michael Kim; Jing Hou; Mark McVey; Young Jin Lee; Arata Tabuchi; Wolfgang M Kuebler; Zhong-Wei Chai; Alan H Lazarus Journal: PLoS One Date: 2012-02-17 Impact factor: 3.240