Apocynin attenuates ventilator-induced lung injury in an isolated and perfused rat lung model

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• 作者：Chi-Huei Chiang (1) (2)
  Chiao-Hui Chuang (1)
  Shiou-Ling Liu (1)
  Tzong-Shyuan Lee (3)
  Yu Ru Kou (3)
  Haibo Zhang (4) (5) (6) (7)
  
• 关键词：ARDS ; Inflammation ; NADPH ; MAPK ; NF ; κB
• 刊名：Intensive Care Medicine
• 出版年：2011
• 出版时间：August 2011
• 年：2011
• 卷：37
• 期：8
• 页码：1360-1367
• 全文大小：610KB
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• 作者单位：Chi-Huei Chiang (1) (2)
  Chiao-Hui Chuang (1)
  Shiou-Ling Liu (1)
  Tzong-Shyuan Lee (3)
  Yu Ru Kou (3)
  Haibo Zhang (4) (5) (6) (7)
  
  1. Division of Pulmonary Immunology and Infectious Diseases, Chest Department, Taipei Veterans General Hospital, No. 201, Section?2, Shih-Pai Road, Taipei, Taiwan
  2. Institute of Emergency and Critical Care Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan
  3. Department and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, Taiwan
  4. The Keenan Research Centre in the Li Ka Shing Knowledge Institute of St. Michael’s Hospital, Toronto, Canada
  5. Department of Anaesthesia, University of Toronto, Toronto, ON, Canada
  6. Department of Physiology, University of Toronto, Toronto, ON, Canada
  7. Interdepartmental Division of Critical Care Medicine, University of Toronto, Toronto, ON, Canada
  

文摘

Rationale Apocynin suppresses the generation of reactive oxygen species (ROS) that are implicated in ventilator-induced lung injury (VILI). We thus hypothesized that apocynin attenuates VILI. Methods VILI was induced by mechanical ventilation with tidal volume (V t) of 15?ml/kg in isolated and perfused rat lung. Apocynin was administered in the perfusate at onset of mechanical ventilation. A group ventilated with low V t of 5?ml/kg served as control. Hemodynamics, lung injury indices, inflammatory responses, and activation of apoptotic pathways were determined upon completion of mechanical ventilation. Results There was an increase in lung permeability and lung weight gain after mechanical ventilation with high V t, compared with low V t. Levels of inflammatory cytokines including interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), and macrophage inflammatory protein-2 (MIP-2) increased in lung lavage fluids; concentrations of carbonyl, thiobarbituric acid reactive substances, and H2O2 were higher in perfusates and lung lavage fluids, and expression of myeloperoxidase, JNK, p38, and caspase-3 in lung tissue was greater in the high-V t than in the low-V t group. Administration of apocynin attenuated these inflammatory responses and lung permeability associated with decreased activation of nuclear factor-κB. Conclusions VILI is associated with inflammatory responses including generation of ROS, cytokines, and activation of mitogen-activated protein kinase cascades. Administration of apocynin at onset of mechanical ventilation attenuates inflammatory responses and VILI in the isolated, perfused rat lung model.