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J Appl Physiol 92: 949-956, 2002. First published October 12, 2001; doi:10.1152/japplphysiol.00776.2001
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Vol. 92, Issue 3, 949-956, March 2002

Low-volume ventilation causes peripheral airway injury and increased airway resistance in normal rabbits

Edgardo D'Angelo1, Matteo Pecchiari1, Paolo Baraggia1, Marina Saetta2, Elisabetta Balestro2, and Joseph Milic-Emili3

1 Istituto di Fisiologia Umana I, Università di Milano, 20133 Milan; and 2 Dipartimento di Medicina Clinica e Sperimentale, Università di Padova, 35128 Padua, Italy; and 3 Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada H2X 2P2

Lung mechanics and morphometry of 10 normal open-chest rabbits (group A), mechanically ventilated (MV) with physiological tidal volumes (8-12 ml/kg), at zero end-expiratory pressure (ZEEP), for 3-4 h, were compared with those of five rabbits (group B) after 3-4 h of MV with a positive end-expiratory pressure (PEEP) of 2.3 cmH2O. Relative to initial MV on PEEP, MV on ZEEP caused a progressive increase in quasi-static elastance (+36%) and airway (Rint; +71%) and viscoelastic resistance (+29%), with no change in the viscoelastic time constant. After restoration of PEEP, quasi-static elastance and viscoelastic resistance returned to control levels, whereas Rint remained elevated (+22%). On PEEP, MV had no effect on lung mechanics. Gas exchange on PEEP was equally preserved in groups A and B, and the lung wet-to-dry ratios were normal. Both groups had normal alveolar morphology, whereas only group A had injured respiratory and membranous bronchioles. In conclusion, prolonged MV on ZEEP induces histological evidence of peripheral airway injury with a concurrent increase in Rint, which persists after restoration of normal end-expiratory volumes. This is probably due to cyclic opening and closing of peripheral airways on ZEEP.

lung elastance; interrupter resistance; viscoelasticity; lung unit recruitment and derecruitment; lung injury scores


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