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Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver
Correspondence: Edward Abraham, M.D., Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Mail Code C-272, 4200 East Ninth Ave., Denver, CO 80262. E-mail: Edward.Abraham{at}UCHSC.edu
Catecholamines are released in high levels after hemorrhage or
endotoxemia and have been shown to modulate immune function, including
cellular release of inflammatory mediators. In the present experiments,
we examined the effects of endogenous and exogenous catecholamines on
neutrophil accumulation and activation in the lungs using pretreatment
with 
- or ß-antagonists or -adrenergic agonists before
hemorrhage or endotoxemia. These studies showed that -, but not
ß-adrenergic stimuli, modulated the severity of acute lung injury
after hemorrhage or endotoxemia, and -adrenergic stimuli was
proinflammatory after hemorrhage but anti-inflammatory after
endotoxemia. The observed -adrenergic effects on lung neutrophil
activation appeared to involve primarily the extracellular
signal-regulated kinase pathway at the upstream kinase Raf, but not
Ras. Although p38 and protein kinase A were activated in lung
neutrophils after hemorrhage or endotoxemia, these kinases were not
affected by - or ß-adrenergic modulation. These results
demonstrate that catecholamines have important immunomodulatory effects
in vivo that affect intracellular signaling pathways in neutrophils and
neutrophil-driven, inflammatory processes such as the development of
acute lung injury.
Key Words: intracellular signaling • Ras • Raf • MEK • ERK • p38 • PKA • -adrenergic stimulation • ß-adrenergic stimulation
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