Publication
Title
N-acetylcysteine pretreatment of cardiac surgery patients influences plasma elastase and neutrophil numbers in bronchoalveolar lavage fluid
Author
Abstract
Objective: Study of leukocyte activation and release of toxic mediators during extracorporeal circulation (EEC). ECC can be used to study the potential protective effect of a pharmacon against neutrophil-mediated lung injury. Clinical studies have indicated that N-acetylcysteine (NAC) may improve systemic oxygenation and reduce the need for ventilatory support when given to patients with acute lung injury. Design: Cardiac surgery patients were pretreated with high-dose NAC in order to assess the potential role of NAC to interfere with neutrophil-mediated inflammation and lung injury. Patients: 18 patients who underwent ECC: group 1 (n = 8) no premedication (only placebo); group 2 (n = 10) NAC (72 mg/kg i.v. as a bolus, later 72 mg/kg over 12 h). Measurements and results: In group 2, the partial pressure of oxygen in arterial blood fractional inspired oxygen 4 h after surgery was significantly higher than in group 1 (213 +/- 31 vs 123 +/- 22; p = 0.044). NAC pretreatment prevented an increase in plasma neutrophil elastase activity (18.9 +/- 6.9 vs 49.9 +/- 5.6 ng/ml in group 1 at the end of ECC; p = 0.027). Release of myeloperoxidase (MPO) was not affected (group 1: 1105 +/- 225 ng/ml vs group 2: 1127 +/- 81 at the end of ECC; p = 0.63). At the end of ECC, total antigenic human neutrophil elastase (group 1: 671 +/- 72 ng/ml vs group 2: 579 +/- 134; p = 0.37) and complex formation between elastase and alpha(1)-proteinase inhibitor were no different in the two groups. There were no significant differences in cellular composition and mediators in the lavage fluid, although values for total number of neutrophils, elastase, MPO and interleukin-8 were lower in group 2. Conclusion: Pretreatment with NAC may prevent lung injury by diminishing elastase activity. Since the release of mediators, especially MPO, is not affected, this diminished activity of elastase may be achieved by enhanced inactivation by antiproteases after initial treatment.
Language
English
Source (journal)
Intensive care medicine. - Heidelberg
Publication
Heidelberg : 1996
ISSN
0342-4642
Volume/pages
22:9(1996), p. 900-908
ISI
A1996VM62200012
Full text (Publishers DOI)
UAntwerpen
Faculty/Department
Research group
Publication type
Affiliation
Publications with a UAntwerp address
External links
Web of Science
Record
Identification
Creation 08.10.2008
Last edited 16.05.2017
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