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Lung. 1987;165(5):305-22.

Lung mechanics, gas exchange, pulmonary perfusion, and hemodynamics in a canine model of acute Pseudomonas pneumonia.

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Department of Medicine, University of Manitoba, Winnipeg, Canada.


Acute bilateral hemorrhagic pneumonia was induced in 6 dogs (pneumonia group) by endotracheal inoculation with Pseudomonas aeruginosa. Measurements of lung mechanics, gas exchange, distribution of pulmonary blood flow, and hemodynamics were made prior to inoculation and 5 hr later when pneumonia was established. These findings were compared to the same measurements in 6 other dogs inoculated with a sterile broth (control group). While there were no significant changes in lung mechanics in the control group, pneumonia caused a significant and proportional reduction (42%) in total lung capacity (TLC) and functional residual capacity (FRC). Although tidal lung compliance was reduced in the pneumonia group, neither the specific compliance nor the deflation pressure-volume curve, with lung volume expressed as a percentage of observed TLC, changed significantly. Pneumonia caused marked hypoxemia with a mean increase in shunt and venous admixture of 35% and 52%, respectively, while the control group developed only minimal abnormalities in gas exchange. Perfusion of the consolidated lung region, determined by radioactive microspheres and expressed as a percentage of total pulmonary blood flow, showed a small but significant decrease from baseline (53 +/- 13%) to established pneumonia (44 +/- 14%), while no change in lobar perfusion was seen in the control group. Only the infected animals showed significant changes in hemodynamics with a rise in cardiac output and fall in mean systemic arterial pressure and vascular resistance. We conclude that acute experimental Pseudomonas pneumonia causes reduction of FRC by filling of alveoli with inflammatory exudate and further reduction of TLC by preventing these alveoli from inflating at higher lung volumes without evidence for a change in the elastic properties of the remaining inflated lung; marked hypoxemia caused by maintenance of perfusion of consolidated lung with reduced or absent ventilation; and a hyperdynamic septic hemodynamic state similar to that seen in humans.

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