The role of endothelin-1 in hyperoxia-induced lung injury in mice

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Serval ID
serval:BIB_4AD03F20146F
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
The role of endothelin-1 in hyperoxia-induced lung injury in mice
Journal
Respiratory Research
Author(s)
Habre  W., Petak  F., Ruchonnet-Metrailler  I., Donati  Y., Tolsa  J. F., Lele  E., Albu  G., Beghetti  M., Barazzone-Argiroffo  C.
ISSN
1465-993X (Electronic)
Publication state
Published
Issued date
2006
Volume
7
Pages
45
Notes
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Abstract
BACKGROUND: As prolonged hyperoxia induces extensive lung tissue damage, we set out to investigate the involvement of endothelin-1 (ET-1) receptors in these adverse changes. METHODS: Experiments were performed on four groups of mice: control animals kept in room air and a group of mice exposed to hyperoxia for 60 h were not subjected to ET-1 receptor blockade, whereas the dual ETA/ETB-receptor blocker tezosantan (TEZ) was administered via an intraperitoneal pump (10 mg/kg/day for 6 days) to other groups of normal and hyperoxic mice. The respiratory system impedance (Zrs) was measured by means of forced oscillations in the anesthetized, paralyzed and mechanically ventilated mice before and after the iv injection of ET-1 (2 microg). Changes in the airway resistance (Raw) and in the tissue damping (G) and elastance (H) of a constant-phase tissue compartment were identified from Zrs by model fitting. RESULTS: The plasma ET-1 level increased in the mice exposed to hyperoxia (3.3 +/- 1.6 pg/ml) relative to those exposed to room air (1.6 +/- 0.3 pg/ml, p < 0.05). TEZ administration prevented the hyperoxia-induced increases in G (13.1 +/- 1.7 vs. 9.6 +/- 0.3 cmH2O/l, p < 0.05) and H (59 +/- 9 vs. 41 +/- 5 cmH2O/l, p < 0.05) and inhibited the lung responses to ET-1. Hyperoxia decreased the reactivity of the airways to ET-1, whereas it elevated the reactivity of the tissues. CONCLUSION: These findings substantiate the involvement of the ET-1 receptors in the physiopathogenesis of hyperoxia-induced lung damage. Dual ET-1 receptor antagonism may well be of value in the prevention of hyperoxia-induced parenchymal damage.
Keywords
Airway Resistance/drug effects Animals Endothelin-1/blood/*pharmacology Female Hyperoxia/*blood/metabolism/physiopathology Lung/*drug effects/metabolism/physiopathology Lung Diseases/*blood/metabolism/physiopathology Mice Mice, Inbred C57BL Models, Biological Pyridines/pharmacology Receptors, Endothelin/drug effects/metabolism Tetrazoles/pharmacology Time Factors Vasodilator Agents/pharmacology
Pubmed
Web of science
Open Access
Yes
Create date
28/01/2008 13:52
Last modification date
20/08/2019 13:58
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