Andrew D Bersten1,2, Malgorzata Krupa2, Kim Griggs2, Dani-Louise Dixon3,4. 1. Intensive and Critical Care Unit, Flinders Medical Centre, Adelaide, SA, Australia. 2. Department of Critical Care Medicine, College of Medicine and Public Health, Flinders University, Adelaide, SA, 5001, Australia. 3. Intensive and Critical Care Unit, Flinders Medical Centre, Adelaide, SA, Australia. dani.dixon@flinders.edu.au. 4. Department of Critical Care Medicine, College of Medicine and Public Health, Flinders University, Adelaide, SA, 5001, Australia. dani.dixon@flinders.edu.au.
Abstract
INTRODUCTION: The mechanism of fast inspiratory flow rate (VI') induced lung injury is unclear. As fast VI' increases hysteresis, a measure of surface tension at the air-liquid interface, surfactant release or function may be important. This experimental study examines the contribution of impaired surfactant release or function to dynamic-VILI. METHODS: Isolated perfused lungs from male Sprague Dawley rats were randomly allocated to four groups: a long or short inspiratory time (Ti = 0.5 s; slow VI' or Ti = 0.1 s; fast VI') at PEEP of 2 or 10 cmH2O. Tidal volume was constant (7 ml/kg), with f = 60 breath/min. Forced impedance mechanics (tissue elastance (Htis), tissue resistance (Gtis) and airway resistance (Raw) were measured at 30, 60 and 90 min following which the lung was lavaged for surfactant phospholipids (PL) and disaturated PL (DSP). RESULTS: Fast VI' resulted in a stiffer lung. Concurrently, PL and DSP were decreased in both tubular myelin rich and poor fractions. Phospholipid decreases were similar with PEEP. In a subsequent cohort, laser confocal microscopy-based assessment demonstrated increased cellular injury with increased VI' at both 30 and 90 min ventilation. CONCLUSION: Rapid VI' may contribute to ventilator induced lung injury (VILI) through reduced surfactant release and/or more rapid reuptake despite unchanged tidal stretch.
INTRODUCTION: The mechanism of fast inspiratory flow rate (VI') induced lung injury is unclear. As fast VI' increases hysteresis, a measure of surface tension at the air-liquid interface, surfactant release or function may be important. This experimental study examines the contribution of impaired surfactant release or function to dynamic-VILI. METHODS: Isolated perfused lungs from male Sprague Dawley rats were randomly allocated to four groups: a long or short inspiratory time (Ti = 0.5 s; slow VI' or Ti = 0.1 s; fast VI') at PEEP of 2 or 10 cmH2O. Tidal volume was constant (7 ml/kg), with f = 60 breath/min. Forced impedance mechanics (tissue elastance (Htis), tissue resistance (Gtis) and airway resistance (Raw) were measured at 30, 60 and 90 min following which the lung was lavaged for surfactant phospholipids (PL) and disaturated PL (DSP). RESULTS: Fast VI' resulted in a stiffer lung. Concurrently, PL and DSP were decreased in both tubular myelin rich and poor fractions. Phospholipid decreases were similar with PEEP. In a subsequent cohort, laser confocal microscopy-based assessment demonstrated increased cellular injury with increased VI' at both 30 and 90 min ventilation. CONCLUSION: Rapid VI' may contribute to ventilator induced lung injury (VILI) through reduced surfactant release and/or more rapid reuptake despite unchanged tidal stretch.
Authors: Nicholas E Vlahakis; Mark A Schroeder; Richard E Pagano; Rolf D Hubmayr Journal: Am J Respir Crit Care Med Date: 2002-11-01 Impact factor: 21.405
Authors: K G Davidson; A D Bersten; H A Barr; K D Dowling; T E Nicholas; I R Doyle Journal: Am J Physiol Lung Cell Mol Physiol Date: 2000-12 Impact factor: 5.464
Authors: Kate G Davidson; Andrew D Bersten; Heather A Barr; Kay D Dowling; Terence E Nicholas; Ian R Doyle Journal: Am J Respir Crit Care Med Date: 2002-06-01 Impact factor: 21.405