Vol. 90, Issue 3, 1049-1056, March 2001
The lung diffusing capacity for nitric oxide in rats is
increased during endotoxemia
John T.
Stitt and
Arthur B.
DuBois
John B. Pierce Laboratory, Yale University School of Medicine, New
Haven, Connecticut 06519
Rats, when injected with endotoxin, begin to
exhale nitric oxide (NO) within 1 h. This study measured the
diffusing capacity for NO in the lungs of rats
(DLNO) under both control and endotoxemic conditions, and it also estimated the rate at which endogenous NO
(
PNO) enters the distal compartment of
the lung, both in control rats and during endotoxemia.
DLNO increased from 0.68 ± 0.12 (SE)
ml · min
1 · mmHg1 in
control rats to 1.17 ± 0.25 ml · min1 · mmHg1 in
endotoxemic rats. PNO was 2.6 ± 0.5 nl/min in control rats and attained a value of 218.6 ± 50.1 nl/min at the height of NO exhalation 3 h after the endotoxin. We
suggest that increased DLNO reflects an
increase in pulmonary membrane diffusing capacity, caused by a
pulmonary hypertension that is due to neutrophil aggregation in the
lung capillaries. DLNO may also be increased by
an enlarged pulmonary capillary volume because of the vasodilatory
effects of the endogenous NO that is produced by the lung in response to the endotoxin. NO production by the lungs in response to endotoxin is unique in that it is the only situation reported to date in which
pathologically induced increases in NO exhalation originate from the
alveolar compartment of the lung, as opposed to the small conducting airways.
adult respiratory distress syndrome; lipopolysaccharides; lung
injury; pulmonary diffusing capacity
