Conclusions
As measured by the luminol enhanced chemiluminescence stimulated by zymosan A the posttraumatic stimulatory response was increased in blood derived and decreased in BAL derived PMNL as compared to normals. This loss of metabolic function is paralleled by an increased extracellular release of respiratory burst products and lysosomal enzymes from stimulated and phagocytosing PMNL during their capillary-interstitial-alveolar passage. These events seem to be part of the pathogenetic mechanisms that contribute to the lung injury in ARDS. The observed shortening of photon emission times is supposed to be caused by C3b receptor affinity and/or concentration increase during the in vivo PMNL stimulation and migration across the blood/air barrier as a result of the attempt to compensate for the disappearing response ability.
Abbreviations
- PTS :
-
polytrauma scale ≙ injury severity score (ISS)
- PBS :
-
phosphate buffered saline
- MEM :
-
minimal essential medium
References
Allen RC, Stjernholm RL, Steele RH (1972) Biochem Biophys Res Commun 47:679
Schraufstatter I, Revak SD, Cochrane CG (1984) Fed Proc 43:2807
Tate RM, Repine JE (1983) Am Rev Resp Dis 128 (3):552
Worthen GS, Henson PM (1983) Clin Lab Med 3:601
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Supported by the “Deutsche Forschungsgemeinschaft” project II B 6
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Dwenger, A., Regel, G. & Schweitzer, G. Pathomechanisms of the adult respiratory distress syndrome (ARDS): Chemiluminescence analysis of polymorphonuclear leukocytes. Z. Anal. Chem. 324, 360–361 (1986). https://doi.org/10.1007/BF00487995
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DOI: https://doi.org/10.1007/BF00487995