Leukocytes Aggregation and Complement Activation in ARDS

  • J. Duchateau
  • M. Braun
  • M. Lamy
Conference paper
Part of the Update in Intensive Care and Emergency Medicine book series (UICM, volume 1)


Diffuse alveolar capillary membrane injury appears to be the initial pathophysiologic feature of ARDS. This results in acute respiratory failure through pulmonary edema. Involvement of polymorphonuclear cells (PMN) as effector cells initiating the vascular injury was proposed by Craddock, Jacob and coworkers [1, 2]. The arguments are based on morphologic observations of the accumulation or sequestration of PMN in the pulmonary vasculature of animal models of ARDS, induced by a veriety of stimuli such as endotoxemia, bacteremia, hemorrhagic shock, cardiopulmonary bypass, complement-activated sera, etc... [reviewed in 3]. Similar observations are pertinent to the clinical situations where PMN accumulation has been documented in the lung microvasculature of ARDS patients. The most suggestive evidence for a key role of PMN is the absence or important reduction of induced pulmonary edema when animals are depleted of their granulocytes. Although the human counterpart is poorly documented in the literature, the development of ARDS in leukopenic patients, and secondary to sepsis for example, seems to be coincidental with bone marrow recovery in PMN release (Dr. D. Bron, personnal communication).


Pulmonary Edema Complement Activation Acute Respiratory Failure Allergy Clin Immunol Adult Respiratory Distress Syndrome 
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Copyright information

© Springer-Verlag Berlin Heidelberg 1986

Authors and Affiliations

  • J. Duchateau
  • M. Braun
  • M. Lamy

There are no affiliations available

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