SC5b-9-Induced Pulmonary Microvascular Endothelial Hyperpermeability Participates in Ventilator-Induced Lung Injury |
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Authors: | Kan Liu Yan-Fei Mao Juan Zheng Zhao-Yun Peng Wen-Wu Liu Yun Liu Wei-Gang Xu Xue-Jun Sun Chun-Lei Jiang Lai Jiang |
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Institution: | 1. Department of Diving Medicine, Faculty of Nautical Medicine, Second Military Medical University, Shanghai, 200433, China 3. Department of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200092, China 2. Department of Nautical Medicine, Faculty of Nautical Medicine, Second Military Medical University, Shanghai, 200433, China
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Abstract: | Mechanical ventilation with large tidal volumes can increase lung alveolar permeability and initiate inflammatory responses, termed ventilator-induced lung injury (VILI). VILI is characterized by an influx of inflammatory cells, increased pulmonary permeability, and endothelial and epithelial cell death. But the underlying molecular mechanisms that regulate VILI remain unclear. The purpose of this study was to investigate the mechanisms that regulate pulmonary endothelial barrier in an animal model of VILI. These data suggest that SC5b-9, as the production of the complement activation, causes increase in rat pulmonary microvascular permeability by inducing activation of RhoA and subsequent phosphorylation of myosin light chain and contraction of endothelial cells, resulting in gap formation. In general, the complement-mediated increase in pulmonary microvascular permeability may participate in VILI. |
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