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Titolo:
Antiinflammatory properties of inducible nitric oxide synthase in acute hyperoxic lung injury
Autore:
Kobayashi, H; Hataishi, R; Mitsufuji, H; Tanaka, M; Jacobson, M; Tomita, T; Zapol, WM; Jones, RC;
Indirizzi:
Kitasato Univ, Sch Med, Dept Med, Sagamihara, Kanagawa 2288555, Japan Kitasato Univ Sagamihara Kanagawa Japan 2288555 , Kanagawa 2288555, Japan Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anaesthesia & Crit Care, Boston, MA 02114 USA Harvard Univ Boston MA USA 02114 thesia & Crit Care, Boston, MA 02114 USA
Titolo Testata:
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
fascicolo: 4, volume: 24, anno: 2001,
pagine: 390 - 397
SICI:
1044-1549(200104)24:4<390:APOINO>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
OXYGEN-TOXICITY; TYROSINE NITRATION; RAT LUNG; PULMONARY-HYPERTENSION; ALVEOLAR MACROPHAGES; MESSENGER-RNA; PROTECTS RATS; MICE; EXPRESSION; PEROXYNITRITE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Kobayashi, H Kitasato Univ, Sch Med, Dept Med, Kitasato 1-15-1 Sagamihara,Sagamihara, Kanagawa 2288555, Japan Kitasato Univ Kitasato 1-15-1 Sagamihara Sagamihara Kanagawa Japan 2288555
Citazione:
H. Kobayashi et al., "Antiinflammatory properties of inducible nitric oxide synthase in acute hyperoxic lung injury", AM J RESP C, 24(4), 2001, pp. 390-397

Abstract

The objective of this study was to determine whether endogenous nitric oxide (NO), specifically the inducible NO synthase isoform (iNOS: NOS II), reduces or amplifies lung injury in mice breathing at a high oxygen tension. Previous studies have shown that exogenous (inhaled) NO protects against hyperoxia-induced lung injury, and that endogenous NO derived from iNOS inhibits leukocyte recruitment and protects against lung injury induced by lipopolysaccharide. In the present study, hyperoxia (> 98% O-2 for 72 h) induced acute lung injury in both wild-type and iNOS-deficient mice as determined by elevated albumin and lactate dehydrogenase levels in bronchoalveolar lavage fluid (BALF) and by increased extravascular lung water. Lung injury was greater in iNOS-deficient mice than in wild-type mice and was associated with an increased number of polymorphonuclear leukocytes in BALF. iNOS messenger RNA expression levels increased in the lungs of wild-type hyperoxic mice. Nitrotyrosine, a marker of reactive NO species, was expressed in both wild-type and iNOS-deficient mice in hyperoxia, indicating an iNOS-independent pathway for protein nitration, We conclude that iNOS is capable of reducing pulmonary leukocyte accumulation and lung injury. The data indicate thatiNOS induction serves as a protective mechanism to minimize the effects ofacute exposure to hyperoxia.

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Documento generato il 03/04/20 alle ore 03:16:26