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Vol. 84, Issue 1, 107-115, January 1998
Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892
Quezado, Zenaide M. N., Charles Natanson, Waheedullah
Karzai, Robert L. Danner, Cezar A. Koev, Yvonne Fitz, Donald P. Dolan, Steven Richmond, Steven M. Banks, Laura Wilson, and Peter Q. Eichacker. Cardiopulmonary effects of inhaled nitric oxide in normal dogs and
during E. coli pneumonia and sepsis.
J. Appl. Physiol. 84(1): 107-115, 1998.
We investigated the effect of inhaled nitric oxide (NO) at
increasing fractional inspired O2
concentrations (FIO2) on
hemodynamic and pulmonary function during Escherichia coli pneumonia. Thirty-eight conscious,
spontaneously breathing, tracheotomized 2-yr-old beagles had
intrabronchial inoculation with either 0.75 or 1.5 × 1010 colony-forming units/kg of
E. coli 0111:B4
(infected) or 0.9% saline (noninfected) in one or four pulmonary
lobes. We found that neither the severity nor distribution (lobar vs.
diffuse) of bacterial pneumonia altered the effects of NO. However, in infected animals, with increasing
FIO2 (0.08, 0.21, 0.50, and
0.85), NO (80 parts/million) progressively increased arterial PO2 [
0.3 ± 0.6, 3 ± 1, 13 ± 4, 10 ± 9 (mean ± SE) Torr, respectively] and decreased the mean arterial-alveolar
O2 gradient (0.5 ± 0.3, 4 ± 2, 8 ± 7, 10 ± 9 Torr, respectively). In
contrast, in noninfected animals, the effect of NO was significantly
different and opposite; NO progressively decreased mean
PO2 with increasing
FIO2 (2 ± 1, 5 ± 3, 2 ± 3, and 12 ± 5 Torr, respectively;
P < 0.05 compared with infected
animals) and increased mean arterial-alveolar
O2 gradient (0.3 ± 0.04, 2 ± 2, 1 ± 3, 11 ± 5 Torr; P < 0.05 compared with infected animals). In normal and infected
animals alike, only at FIO2
0.21 did NO significantly lower mean pulmonary artery pressure,
pulmonary artery occlusion pressure, and pulmonary vascular resistance
index (all P < 0.01).
However, inhaled NO had no significant effect on increases in mean
pulmonay artery pressure associated with bacterial pneumonia. Thus,
during bacterial pneumonia, inhaled NO had only modest effects on
oxygenation dependent on high
FIO2 and did not affect
sepsis-induced pulmonary hypertension. These data do not support a role
for inhaled NO in bacterial pneumonia. Further studies are necessary to
determine whether, in combination with ventilatory support, NO may have
more pronounced effects.
Escherichia coli; hypoxemia; fractional inspired oxygen; pulmonary artery pressure
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