Exhalation of gaseous nitric oxide by rats in response to endotoxin and its absorption by the lungs.
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 i.v., 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 approximately 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.
Stitt
J T
JT
John B. Pierce Foundation Laboratory, Yale University School of Medicine, New Haven, Connecticut 06519, USA.
Dubois
A B
AB
Douglas
J S
JS
Shimada
S G
SG
D000818:Animals; D004305:Dose-Response Relationship, Drug; D004731:Endotoxins / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D011659:Pulmonary Gas Exchange / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley
D004731:Endotoxins; D009569:Nitric Oxide