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Human polymorphonuclear leukocyte metabolism and lipoperoxidation during adult respiratory distress syndrome treated by extracorporeal carbon dioxide removal

Authors
Publisher
Elsevier Ireland Ltd
Publication Date
Volume
1
Issue
1
Identifiers
DOI: 10.1016/s0928-4680(05)80004-5
Keywords
  • Malondialdehyde
  • Lipoperoxidation
  • Glutathione Peroxidase
  • Oxygen Metabolism
Disciplines
  • Biology

Abstract

Abstract Circulating polymorphonuclear leukocyte (PMNs) oxidative metabolism and lipoperoxidation were evaluated in patients with the adult respiratory distress syndrome (ARDS) treated with low-frequency positive-pressure ventilation and extracorporeal carbon dioxide removal. Chemiluminescence (CL) of resting PMNs from ARDS patients was significantly enhanced relative to controls ( P < 0.001). A significant decrease in CL of resting PMNs from ARDS patients was observed after cell incubation with serum from ARDS patients and healthy controls ( P < 0.05). CL of normal opsonized zymosan (OZ)-stimulated PMNs was significantly enhanced ( P < 0.01) after preincubation with ARDS serum. A significant decrease ( P < 0.05) in control PMN O 2− production was observed after pre-incubation with normal and ARDS serum. Plasma malondialdehyde (MDA) and α 1 proteinase inhibitor-elastase levels were significantly increased in ARDS patients plasma ( P < 0.05), whereas erythocyte glutathione peroxidase was significantly higher in patients who survived ARDS episodes than in those who died ( P < 0.01). CL of resting ARDS PMNs correlated with elastase levels ( r = 0.824; P < 0.001), and MDA levels correlated with the ‘injury severity score’ ( r = 0.46; P = 0.056). Our results show that oxygen metabolism and plasma elastase levels in circulating PMNs from ARDS patients are significantly enhanced. Furthermore, ARDS PMN functions are not enhanced by exogenous stimuli. No correlation between PMN functions and peroxidation was found in ARDS sera. These findings confirm that PMNs are primed during ARDS, but free radical production seems to be only one of the events responsible for the increased lipoperoxidation.

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