Journal of Applied Physiology  AJP: Regulatory, Integrative and Comparative Physiology
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J Appl Physiol (June 12, 2008). doi:10.1152/japplphysiol.90328.2008
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Submitted on February 26, 2008
Revised on June 9, 2008
Accepted on June 11, 2008

The bimodal quasi-static and dynamic elastance of the murine lung

Graeme R Zosky1*, Tibor Z. Janosi, Agnes Adamicza2, Elizabeth M Bozanich3, Vincenzo Cannizzaro1, Alexander N Larcombe, Debra Jane Turner4, Peter D. Sly5, and Zoltan Hantos2

1 University of Western Australia
2 University of Szeged
3 Telethon Institute for Child Health Research and Centre for Child Health Research, University of Western Australia, Perth
4 Institute for Child Health Research
5 Telethon Institute for Child Health Research

* To whom correspondence should be addressed. E-mail: graemez{at}ichr.uwa.edu.au.

The double sigmoidal nature of the mouse PV curve is well recognised but largely ignored. This study systematically examined the effect of inflating the mouse lung to 40 cmH2O transrespiratory pressure (Prs) in vivo. Adult BALB/c mice were anaesthetised, tracheostomised and mechanically ventilated. Thoracic gas volume was calculated using plethysmography and electrical stimulation of the intercostal muscles. Lung mechanics were tracked during inflation-deflation manoeuvres using a modification of the forced oscillation technique. Inflation beyond 20 cmH2O caused a shift in subsequent PV curves with an increase in slope of the inflation limb and an increase in lung volume at 20 cmH2O. There was an overall decrease in tissue elastance and a fundamental change in its volume dependence. This apparent 'softening' of the lung could be recovered by partial degassing of the lung or applying a negative transrespiratory pressure such that lung volume decreased below FRC. Allowing the lung to spontaneously recover revealed that the lung required ~1 hour of mechanical ventilation to return to the original state. We propose a number of possible mechanisms for these observations and suggest that they are most likely explained by the unfolding of alveolar septa and the subsequent redistribution of the fluid lining the alveoli at high transrespiratory pressure.







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