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Titolo:
Effects of endogenous and exogenous catecholamines on LPS-induced neutrophil trafficking and activation
Autore:
Abraham, E; Kaneko, DJ; Shenkar, R;
Indirizzi:
Univ Colorado, Hlth Sci Ctr, Div Pulm Sci & Crit Care Med, Denver, CO 80262 Univ Colorado Denver CO USA 80262 m Sci & Crit Care Med, Denver, CO 80262
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 1, volume: 20, anno: 1999,
pagine: L1 - L8
SICI:
1040-0605(199901)20:1<L1:EOEAEC>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; RESPIRATORY-DISTRESS SYNDROME; BRONCHOALVEOLAR LAVAGE FLUID; FACTOR-ALPHA PRODUCTION; CYCLIC-AMP; LEUKOCYTE ADHESION; GENE-TRANSCRIPTION; ENDOTHELIAL-CELLS; HUMAN ENDOTOXEMIA;
Keywords:
lipopolysaccharide; alpha-adrenergic; beta-adrenergic; acute lung injury; propranolol; phentolamine; UK-14304; phenylephrine; nitric oxide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Abraham, E Univoxolorado, Hlth Sci Ctr, Div Pulm Sci & Crit Care Med, 4200E 9th Ave,B Univ Colorado 4200 E 9th Ave,Box C-272 Denver CO USA 80262 ve,B
Citazione:
E. Abraham et al., "Effects of endogenous and exogenous catecholamines on LPS-induced neutrophil trafficking and activation", AM J P-LUNG, 20(1), 1999, pp. L1-L8

Abstract

Endotoxemia produces elevations in catecholamine levels in the pulmonary and systemic circulation as well as rapid increases in neutrophil number andproinflammatory cytokine expression in the lungs. In the present experiments, we examined the effects of endogenous and exogenous adrenergic stimulation on endotoxin-induced lung neutrophil accumulation and activation. Levels of interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, and macrophage inflammatory protein (MIP)-2 mRNAs were increased in lung neutrophils from endotoxemic mice compared with those present in lung neutrophils from control mice or in peripheral blood neutrophils from endotoxemic or controlmice. Treatment with the beta-adrenergic antagonist propranolol before endotoxin administration did plot affect trafficking of neutrophils to the lungs or the expression of IL-1 beta, TNF-alpha, or MIP-2 by lung neutrophils. Administration of the alpha-adrenergic antagonist phentolamine before endotoxemia did not alter lung neutrophil accumulation as measured by myeloperoxidase (MPO) levels but did result in significant increases in IL-1 beta, TNF-alpha, and MIP-2 mRNA expression by lung neutrophils compared with endotoxemia alone. Administration of the alpha(1)-adrenergic agonist phenylephrine before endotoxin did not affect trafficking of neutrophils to the lungs but was associated with significantly increased expression of TNF-alpha andMIP-2 mRNAs by lung neutrophils compared with that found after endotoxin alone. In contrast, treatment with the alpha(2)-adrenergic agonist UK-14304 prevented endotoxin-induced increases in lung MPO and lung neutrophil cytokine mRNA levels. The suppressive effects of UK-14304 on endotoxin-induced increases in lung MPO were not affected by administration of the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester. These data demonstrate that the initial accumulation and activation of neutrophils in the lungs after endotoxemia can be significantly diminished by alpha(2)-adrenergic stimulation. Therapy with alpha(2)-adrenergic agents may have a role in modulating inflammatory pulmonary processes associated with sepsis-induced acutelung injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 06:51:45