Advertisement

Leukocytes Aggregation and Complement Activation in ARDS

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

Abstract

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).

Keywords

Pulmonary Edema Complement Activation Acute Respiratory Failure Allergy Clin Immunol Adult Respiratory Distress Syndrome 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Craddock PR, Fehr J, Brigham KL, Kronenberg RS, Jacob HS (1977) Complement and leukocyte mediated pulmonary dysfunction in hemodialysis. N Engl J Med 296: 769–774PubMedCrossRefGoogle Scholar
  2. 2.
    Jacob HS, Craddock PR, Hammerschmidt DE, Moldow CF. (1980) Complement induced granulocyte aggregation. An unsuspected mechanism of disease. N Engl J Med 302: 789–794Google Scholar
  3. 3.
    Glauser FL, Fairman RP. (1985) The uncertain role of the neutrophil in increased permeability pulmonary edema. Chest 88: 601–607PubMedCrossRefGoogle Scholar
  4. 4.
    Fearon DT. (1983) Complement. J Allergy Clin Immunol 71: 520–529CrossRefGoogle Scholar
  5. 5.
    Jacob HS, Moldow CF, Flynn PF, Weisdorf DJ, Vercellotti G, Hammerschmidt DE (1982) Therapeutic ramifications of the interaction of complement, granulocytes and platelets in the production of acute lung injury. Ann N-Y Acad Sc 77: 488–495Google Scholar
  6. 6.
    Hammerschmidt DE, Harris PD, Wayland H, Craddock PR, Jacob HS (1981) Complement induced granulocyte aggregation in vivo. Ann J Pathol 102: 146–150Google Scholar
  7. 7.
    Duchateau J, Haas M, Schreyen H, Radoux L, Sprangers I, Noel FX, Braun M, Lamy M (1984) Complement activation in patients at risk of developing the adult respiratory distress syndrome. Am Rev Respir Dis 30: 1058–1064Google Scholar
  8. 8.
    Zimmerman GA, Renzetti AD, Hill HR: (1983) Functional and metabolic activity of granulocytes from patients with adult respiratory distress syndrome. Am Rev Respir Dis 127: 290–300PubMedGoogle Scholar
  9. 9.
    Zimmerman JJ, Shelhamer JH, Parillo JE (1985) Quantitative analysis of polymorphonuclear leukocyte superoxide anion generation in critically ill children. Crit Care Med 13 (3): 143–150PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1986

Authors and Affiliations

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

There are no affiliations available

Personalised recommendations