ERJ
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Order Full text via Infotrieve
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wagner, P.
Right arrow Articles by Glennow, C
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wagner, P.
Right arrow Articles by Glennow, C
Eur Respir J 1989; 2: 116-126
Copyright © ERS Journals Ltd 1989

Original Articles

Protection against pulmonary O2 toxicity by N-acetylcysteine

PD Wagner, O Mathieu-Costello, DE Bebout, AT Gray, PD Natterson, and C Glennow

N-acetylcysteine (NAC) is a known antioxidant. We therefore investigated NAC as an agent protective against O2 toxicity in the lung. Twelve dogs were anaesthetized with sodium pentobarbital and ventilated with 100% O2 for 54 h. Five were given diluent and 7 intravenous NAC (loading dose prior to 100% O2 ventilation of 150 mg.kg-1 and maintenance dose of 20 mg.kg-1.h-1). Every 6 h, physiological evaluation of the pulmonary circulation, mechanical properties, and gas exchange was performed. Post-mortem evaluation consisted of gross examination and weighing followed by light and electron microscopy. By both functional and structural criteria, NAC protected against the effects of 100% O2. The NAC group developed significantly less increase in pulmonary vascular resistance, arterial carbon dioxide tension (PaCO2) and lung wet weight, while dynamic compliance was greater. NAC also delayed the development of abnormal ventilation-perfusion relationships and was associated with reduced pulmonary white cell accumulation, with less evidence of alveolar and interstitial oedema. NAC may well be worthy of evaluation as a therapeutic agent in human diseases characterized by oxidant damage.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
S. Carnevali, S. Petruzzelli, B. Longoni, R. Vanacore, R. Barale, M. Cipollini, F. Scatena, P. Paggiaro, A. Celi, and C. Giuntini
Cigarette smoke extract induces oxidative stress and apoptosis in human lung fibroblasts
Am J Physiol Lung Cell Mol Physiol, June 1, 2003; 284(6): L955 - L963.
[Abstract] [Full Text] [PDF]

Home page
 Arch SurgHome page
E. M. Bulger and R. V. Maier
Antioxidants in Critical Illness
Arch Surg, October 1, 2001; 136(10): 1201 - 1207.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
B. Nemery, A. Bast, J. Behr, P.J.A. Borm, S.J. Bourke, Ph. Camus, P. De Vuyst, H.M. Jansen, V.L. Kinnula, D. Lison, et al.
Interstitial lung disease induced by exogenous agents: factors governing susceptibility
Eur. Respir. J., July 1, 2001; 18(32_suppl): 30S - 42s.
[Abstract] [Full Text] [PDF]

Home page
 Hum Exp ToxicolHome page
J. Meulenbelt, L. van Bree, J.A.M.A. Dormans, and B. Sangster
No Beneficial Effect of N-acetylcysteine Treatment on Broncho-alveolar Lavage Fluid Variables in Acute Nitrogen Dioxide Intoxicated Rats
Human and Experimental Toxicology, January 1, 1994; 13(7): 472 - 477.
[Abstract] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1989 by the European Respiratory Society.