Abstract
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.
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