P479The induction of mild hypothermia prevents acute pulmonary failure during endotoxemia in pigs

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Acute respiratory failure is a major component of multi-organ dysfunction during sepsis. The induction of mild hypothermia (MH, 33 °C) reduces whole body oxygen demand (WB-VO2) and exerts anti-inflammatory effects in experimental settings. We tested effects of MH during endotoxemia in pigs.


Anesthetized pigs (65 ± 2 kg) were acutely instrumented (closed chest) with a series of catheters including an intravascular cooling device, and were ventilated in a volume controlled mode (tidal volume=10 ml/kg, FiO2=50%). Respiratory rate was adjusted to keep end-tidal pCO2 at 40-45 mmHg. Endotoxemia, a model of septic shock, was induced by lipopolysaccharid (LPS) infusion at 0.5 µg/kg/h for 1h and 1 µg/kg/h for further 3h. With the beginning of LPS infusion, pigs were assigned to either normothermia (NT, 38 °C, n=7) or MH (33 °C, n=6). Data are reported at 8h after onset of LPS-infusion vs baseline. *: p < 0.05 vs baseline, †: p < 0.05 vs NT.


Heart rate (bpm) increased in NT (128 ± 6* vs 97 ± 4), but decreased in MH (79 ± 4*,† vs 98 ± 4). Mean aortic pressure (mmHg) decreased in NT (53 ± 4* vs 86 ± 2) and MH (58 ± 1* vs 85 ± 2). WB-VO2 and respiratory minute volume (RMV) increased in NT but fell markedly in MH. Arterial oxygen saturation (sO2,art) fell significantly in NT but not in MH. Mixed venous sO2, a strong predictor of mortality during sepsis, was better preserved in MH.


MH prevents acute respiratory failure during endotoxemia. This may relate to (i) reduced systemic oxygen demand with subsequently less ventilation-associated mechanical pulmonary stress and (ii) an anti-inflammatory effect of MH that preserves the lungs capability to oxygenate blood. MH may be a therapeutic option for acute pulmonary failure during sepsis.

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