Because inflammation stimulates the expression of inducible nitric oxide (N
O) synthase (iNOS) with an associated increased local NO production, we hyp
othesized that patients with pneumonia would have increased excretion of NO
into their airways. To test this hypothesis, NO was measured in the exhale
d air and from the nasal cavities of 49 consecutively intubated and mechani
cally ventilated patients in our ICU. After excluding NO gas contamination
in the inspiratory circuit, nasal NO and end-expiratory and mean exhaled tr
acheal NO levels and plasma nitrate concentrations were measured using a fa
st response chemiluminescence analyzer. Twenty-one patients (43%) presented
with infectious pneumonia. End-expiratory exhaled NO concentrations were s
ignificantly higher in patients with pneumonia as compared with patients wi
thout pneumonia (5.9 +/- 1 ppb versus 3.2 +/- 0.5 ppb, p < 0.01). Similarly
, mean nasal NO was higher in patients with pneumonia (1039 +/- 138 ppb ver
sus 367 +/- 58 ppb, p = 0.003). Plasma nitrate levels did not differ betwee
n patient groups. Threshold values of tracheal or nasal NO were defined and
subsequently Validated in 60 other patients. Positive and negative values
of a maximal tracheal level > 5 ppb for pneumonia were 74% and 89%, respect
ively. Thus tracheal and nasal NO levels may be of help in distinguishing p
atients with acute pneumonia from other causes. Furthermore, because these
differences in airway NO levels were not paralleled in blood nitrite concen
trations, we conclude that pneumonia per se is not associated with systemic
NO production.