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,
Departments of
*
Anesthesia,
Medicine, and
Surgery, and
Cardiovascular Research Institute, University of California San Francisco, CA 94110; and
¶
Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706
Our recent experimental work demonstrated that a
neutrophil-dependent inflammatory response in the lung prevented the
normal up-regulation of alveolar fluid clearance by catecholamines
following hemorrhagic shock. In this study, we tested the hypothesis
that the release of NO within the airspaces of the lung was responsible
for the shock-mediated failure of the alveolar epithelium to respond to
catecholamines in rats. Hemorrhagic shock was associated with an
inducible NO synthase (iNOS)-dependent increase in the lung production
of NO and a failure of the alveolar epithelium to up-regulate vectorial
fluid transport in response to 
-adrenergic agonists. Inhibition of
iNOS restored the normal catecholamine-mediated up-regulation of
alveolar liquid clearance. Airspace instillation of dibutyryl cAMP, a
stable analog of cAMP, restored the normal fluid transport capacity of
the alveolar epithelium after prolonged hemorrhagic shock, whereas
direct stimulation of adenyl cyclase by forskolin had no effect.
Pretreatment with pyrrolidine dithiocarbamate or sulfasalazine
attenuated the iNOS-dependent production of NO in the lung and restored
the normal up-regulation of alveolar fluid clearance by catecholamines
after prolonged hemorrhagic shock. Based on in vitro studies with an
alveolar epithelial cell line, A549 cells, the effect of sulfasalazine
appeared to be mediated in part by inhibition of NF-
B activation,
and the protective effect was mediated by the inhibition of IB
protein degradation. In summary, these results provide the first in
vivo evidence that NO, released within the airspaces of the lung
probably secondary to the NF-B-dependent activation of iNOS, is a
major proximal inflammatory mediator that limits the rate of alveolar
epithelial transport after prolonged hemorrhagic shock by directly
impairing the function of membrane proteins involved in the
-adrenergic receptor-cAMP signaling pathway in alveolar
epithelium.
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