Pathomechanisms of the adult respiratory distress syndrome (ARDS): elastase contents of polymorphonuclear leukocytes and elastase release during passage across the blood/air barrier

Conclusions

In comparison to normals blood derived PMNL of ARDS patients were found to be partially depleted of elastase that in turn caused a 5-fold elevation of the plasma elastase concentration. During their capillary-interstitial-alveolar passage stimulated PMNL released elastase as could be demonstrated by the further decreased elastase contents of BAL derived PMNL and by a 68-fold increase in total elastase concentration in BAL fluid as compared to normals. Urea served as an internal reference substance in plasma and BAL fluid as well as the albumin/urea ratios indicated the extent of permeability increase. By this it was possible to judge whether the high total elastase concentration in BAL fluid predominantly resulted from a₁PI-elastase complex permeation or from elastase release during PMNL migration followed by consecutive complexation with ubiquitously occurring a₁PI. The total elastase/urea ratios of the patients were elevated 79-fold above normals in BAL fluid whereas the patients' albumin/urea ratios were only 4.4-fold higher than those of normals. These data gave evidence that the high BAL fluid elastase concentration was mainly the result of free elastase release from migrating and phagocytosing PMNL. Hereby, the inflammatory cascades can be started and/ or enhanced, thus contributing to lung injury in ARDS, especially, if non-complexed enzymatically active elastase is present in BAL fluid.