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The John B. Pierce Foundation Laboratory, Yale University School of Medicine, New Haven, Connecticut 06519
Received 9 April 1996; accepted in final form 10 September 1996.
Stitt, John T., Arthur B. DuBois, James S. Douglas, and
Steven G. Shimada. Exhalation of gaseous nitric oxide by rats in
response to endotoxin and its absorption by the lungs.
J. Appl. Physiol. 82(1): 305-316, 1997.
Rats injected with a lipopolysaccharide endotoxin produce
detectable concentrations of nitric oxide gas (NO) in the expired air
within 60 min. The concentration of NO reaches a plateau at 3 h. Production of the NO is dose dependent on
lipopolysaccharide, and at a dose of 1 mg/kg iv, lipopolysaccharide alveolar concentrations of >260 parts per billion are observed. NO
synthase inhibitors suppress this NO production in response to
endotoxin. Experiments were conducted to ascertain the site of origin
of this NO and to measure the capacity of the lungs to absorb NO from
alveolar air. Results indicate that the endotoxin-induced NO originates
from within the lungs themselves and that the lungs have the capacity
to absorb >60% of NO that is presented to them. Lung tissues absorb
~44-47% of the NO load, blood carries away between 15 and 19%,
while the remainder is exhaled in the expired air. It is proposed that
the exhalation of NO might prove useful as an early biomarker for acute
lung injury.
lung injury; neutrophils; endothelial cells
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