Abstract 6: The Induction of Mild Hypothermia Prevents Acute Respiratory Failure During Endotoxemia in Pigs
Background: Acute respiratory failure is a major component of multi-organ failure during sepsis. The induction of mild hypothermia (MH, 33 °C) reduces whole body oxygen demand and exerts anti-inflammatory effects in experimental settings. We tested the effect of MH on respiratory function during experimental endotoxemia in pigs.
Methods: Anesthetized pigs (65±2 kg) were acutely instrumented (closed chest) with a series of catheters (Swan-Ganz catheter, left ventricular pressure-volume catheter, intravascular cooling device). Pigs were ventilated in a volume controlled mode at a tidal volume of 10 ml/kg (FiO2 50%). Respiratory rate was adjusted to keep end-tidal pCO2 between 40 and 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) and followed for a total of 8 hours. Data are reported at 8h after onset of LPS-infusion vs baseline. *: p<0.05 vs baseline, †: p<0.05 vs NT.
Results: 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 to the same degree in NT (53±4* vs 86±2) and MH (58±1* vs 85±2). Whole body oxygen consumption (WB-VO2) increased during LPS infusion in NT but fell markedly in MH (see graph). Respiratory minute volume (RMV) changed accordingly in the two groups. Moreover, arterial oxygen saturation (sO2,art) fell significantly in NT but was almost completely preserved in MH.
Conclusion: MH prevents acute respiratory failure during endotoxemia. This may relate to (i) reduced systemic oxygen demand with subsequently less mechanical pulmonary stress associated with mechanical ventilation and (ii) a direct anti-inflammatory effect of MH that preserves the lungs capability to oxygenate blood. These data imply that MH may be a therapeutic option for acute pulmonary failure during sepsis.
- © 2011 by American Heart Association, Inc.