Vascular hyperpermeable molecules potentially contributing to the development of pulmonary edema in sepsis-associated ARDS

  • Hattori Kohshi
    Department of Anesthesiology, Center Hospital of the National Center for Global Health and Medicine
  • Matsuda Naoyuki
    Department of Emergency and Critical Care Medicine, Nagoya University Graduate School of Medicine
  • Hattori Yuichi
    Advanced Research Promotion Center, Health Sciences University of Hokkaido

Bibliographic Information

Other Title
  • 敗血症性急性呼吸窮迫症候群(ARDS)における肺水腫形成に寄与する血管透過性増大因子

Abstract

<p>The acute respiratory distress syndrome (ARDS) is an important cause of respiratory failure in critically ill patients and may become a life-threatening condition where inflammation of the lungs may begin in one lung but eventually affects both, leading to damage to the alveoli and surrounding small blood vessels. ARDS is particularly characterized by noncardiogenic pulmonary edema caused by an increase in pulmonary capillary permeability. Several clinical disorders can precipitate in ARDS, including pneumonia, sepsis, aspiration of gastric contents, and major trauma. The most common cause of ARDS is sepsis, which is a serious and widespread infection of the bloodstream and is now defined as life-threatening organ dysfunction due to a dysregulated reponse of the host to infection. In sepsis, a number of vascular hyperpermeable factors, such as histamine, nitric oxide, thromboxane A2, and vascular endothelial growth factor, can be overproducted and contribute to the development of pulmonary edema. Given that sepsis can be regarded as a gene-related disorder, the nucleic-acid based gene therapeutic strategy to regulate some transcription factors involved in expression of vascular hyperpermeable genes may be considered to be a promising novel approach for treatment of ARDS in sepsis.</p>

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