Quezado, Zenaide M. N.;
Natanson, Charles;
Karzai, Waheedullah;
Danner, Robert L.;
Koev, Cezar A.;
Fitz, Yvonne;
Dolan, Donald P.;
Richmond, Steven;
Banks, Steven M.;
Wilson, Laura;
Eichacker, Peter Q.
Cardiopulmonary effects of inhaled nitric oxide in normal dogs and during E. coli pneumonia and sepsis
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Medientyp:
E-Artikel
Titel:
Cardiopulmonary effects of inhaled nitric oxide in normal dogs and during E. coli pneumonia and sepsis
Beteiligte:
Quezado, Zenaide M. N.;
Natanson, Charles;
Karzai, Waheedullah;
Danner, Robert L.;
Koev, Cezar A.;
Fitz, Yvonne;
Dolan, Donald P.;
Richmond, Steven;
Banks, Steven M.;
Wilson, Laura;
Eichacker, Peter Q.
Beschreibung:
<jats:p> 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 O<jats:sub>2</jats:sub>concentrations ([Formula: see text]) 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 × 10<jats:sup>10</jats:sup> 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[Formula: see text] (0.08, 0.21, 0.50, and 0.85), NO (80 parts/million) progressively increased arterial[Formula: see text] [−0.3 ± 0.6, 3 ± 1, 13 ± 4, 10 ± 9 (mean ± SE) Torr, respectively] and decreased the mean arterial-alveolar O<jats:sub>2</jats:sub> 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[Formula: see text] with increasing[Formula: see text] (2 ± 1, −5 ± 3, −2 ± 3, and −12 ± 5 Torr, respectively; P < 0.05 compared with infected animals) and increased mean arterial-alveolar O<jats:sub>2</jats:sub> 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 [Formula: see text]≤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[Formula: see text] 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. </jats:p>