Abstract
To assess the pathophysiology of pulmonary air leaks, we studied orotracheally intubated mice on mechanical ventilation with pleural injuries produced by a 25g needle inserted 1–2 mm into the lung parenchyma. The pleural injuries were studied using a standard inflation maneuver involving a 3 second ramp to 30 cmH20 followed by a 3 second breath hold. After pleural injury, the inflation maneuver resulted in a distinctive airway pressure time history; that is, peak inflation was followed by a rapid decrease to a lower plateau phase. The decay phase of the inflation maneuver was influenced by the injury area; the rate of pressure decline with multiple injuries (28+8 cmH20/sec) was significantly greater than a single injury (12+3 cmH20/sec)(p<.05). In contrast, the plateau phase pressure was independent of injury surface area, but dependent upon transpulmonary pressure. When the standard inflation maneuver was performed in a pressure‐regulated body box, the plateau transpulmonary pressures were a mean of 18+0.7 cm H2O regardless of the absolute pressures outside of the lung. Although the pleural injury resulted in a significant increase in delivered air volume (p<.01), there was no significant difference in air leak volume between 1 and 5 injuries (p>.05). These findings are consistent with the regulation of pleural air leaks by transpulmonary pressure‐dependent airway closure.Support or Funding InformationNIH Grant HL94567, HL134229, HL007734, CA009535, ES000002 and the German Research Foundation (SFB1066)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Published Version
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