Intrapulmonary growth of Staphylococcus aureus in rats during induced atelectasis.
Intrinsic pulmonary antibacterial defenses are mediated by alveolar macrophages and by noncellular factors. Mechanical ventilation in the resting tidal volume range leads to alterations in the physical characteristics of alveolar surfactant, alveolar instability, regional hypoxia, and systemic hypoxemia. While a number of experimental manipulations diminish the activity of the intrinsic antibacterial defense system, the effects of mechanical ventilation per se have not been systematically evaluated previously. We found that normal rats ventilated without sighing (periodic large breaths) manifested severe defects in pulmonary clearance of Staphylococcus aureus during 6-h experiments, such that growth of the inoculum occurred. Addition of a timer-controlled mechanism to cause the animals to sigh every 2 min, without other modifications in the experimental conditions, caused significant improvement in clearance. Analysis of cellular response, compartmentalization of viable bacteria, surfactant quantities and sedimentation characteristics, and protein influx indicated that the defect in clearance paralleled alterations in the physical state of surfactant and alveolar stability but was not strongly correlated with alterations in the other parameters we measured. The data show that defective pulmonary bacterial clearance is rapidly induced by measures which alter alveolar stability and suggest that intrinsic pulmonary defenses require maintenance of normal air-liquid interfaces for optimal function.
Frederick
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Department of Internal Medicine, University of Connecticut, Farmington 06037.
Pesanti
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D000818:Animals; D001784:Blood Gas Analysis; D001992:Bronchoalveolar Lavage Fluid / Q000032:analysis; D006358:Hot Temperature; D000860:Hypoxia; D008168:Lung / Q000382:microbiology*; D008170:Lung Compliance; D008264:Macrophages / Q000502:physiology; D008297:Male; D009079:Mucociliary Clearance; D009504:Neutrophils / Q000502:physiology; D001261:Pulmonary Atelectasis / Q000276:immunology* / Q000382:microbiology; D011663:Pulmonary Surfactants / Q000502:physiology*; D051381:Rats; D013211:Staphylococcus aureus / Q000254:growth & development*; D013990:Tidal Volume
D011663:Pulmonary Surfactants