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  • Poster presentation
  • Open Access

Mild hypothermia was protective in a physiological model of ventilator-induced lung injury by reducing inflammation but not by reducing the respiratory rate

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Critical Care201014 (Suppl 1) :P195

  • Published:


  • Public Health
  • Animal Model
  • Respiratory Rate
  • Emergency Medicine
  • Lung Injury


In animal models of ventilator-induced lung injury (VILI), mild hypothermia was found to be protective by reducing pulmonary inflammation and possibly by reducing mechanical strain by applying lower respiratory rates. However, models are hampered by severe alkalosis or an ex vivo design. In a physiological model of VILI, we investigated whether hypothermia protects from VILI by reducing respiratory rates, or by reducing inflammation.


In rats, VILI was induced using a peak inspiratory pressure (PIP) of 23 cmH2O and zero PEEP. Controls were ventilated with a PIP of 12 cmH2O and PEEP of 5 cmH2O. Hypothermia (32ºC) was induced by external cooling, controls were maintained at 37ºC. Normo-pH (7.3 to 7.4) or strict normocapnia (4.5 to 5.0 kPa) was achieved by adjusting the respiratory rate according to blood gases drawn every 30 minutes. After 4 hours of ventilation, bronchoalveolar lavage (BAL) was done. Statistics include Kruskal-Wallis and Mann-Whitney U tests.


A physiological model of VILI was established. In the normo-pH group, hypothermia decreased pulmonary IL-6 and neutrophil influx and tended to decrease pulmonary protein leak (Figure 1). In the normocapnia group, hypothermia allowed for lower respiratory rates compared with normo-pH (11 ± 1 vs 17 ± 2 breaths/minute) (Figure 2). However, this did not further reduce parameters of lung injury.


Hypothermia was protective in a physiological model of VILI, by reduction of inflammation, but not by reducing the repetitive strain of respiratory cycles.

Authors’ Affiliations

Laboratory of Experimental Intensive Care and Anesthesiology, Amsterdam, Netherlands


© BioMed Central Ltd. 2010