Abstract 109: The Induction of Mild Hypothermia Prevents Sympathetic Activation but Preserves Systemic Vascular Resistance During Endotoxemia in Pigs
Background: The induction of mild hypothermia (MH) accelerates the decrease of sympathetic activation after return of spontaneous circulation in pigs resuscitated from ventricular fibrillation. We tested whether or not MH attenuates sympathetic activation during experimental endotoxemia.
Methods: Anesthetized pigs (65±2 kg) were acutely instrumented (closed chest) with a series of catheters including a Swan-Ganz catheter, a left ventricular pressure-volume catheter and an intravascular cooling device. Endotoxemia, a model of septic shock, was induced by lipopolysaccharid (LPS) infusion at 0.5 µg/kg/h for 1 hour and 1 µg/kg/h for further 3 hours. With the beginning of LPS infusion, pigs were assigned to either normothermia (NT, 38 °C, n=7) or MH (33 °C, n=6). Sympathetic activation was assessed by spectral analysis of heart rate variability (HRV) deciphering the high frequency (HF) and low frequency (LF) components of HRV. Animals were 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: Cardiac output (l/min) decreased in MH (4.5±0.5*,† vs 6.2±0.3), but not in NT (6.6±0.4 vs 6.8±0.2). As MH increased systemic vascular resistance (SVR), mean aortic pressure (mmHg) was decreased to similar levels in NT (53±4* vs 86±2) and MH (58±1* vs 85±2). Heart rate increased in NT but fell in MH. The HF component of HRV (=parasympathicus) increased in MH, but decreased in NT. Vice versa, the ratio of HF/LF (=sympathicus) increased in NT, but fell in MH.
Conclusion: The induction of MH during experimental endotoxemia completely prevents sympathetic activation at improved vascular resistance. These data imply that MH may serve to prevent sympathetic overstimulation and vascular paralysis during sepsis.
- © 2011 by American Heart Association, Inc.