P333The induction of mild hypothermia prevents sympathetic activation and improves myocardial beta-adrenergic responsiveness during endotoxemia in pigs

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The induction of mild hypothermia (MH) increases contractility and decreases sympathetic activation after resuscitation from cardiac arrest in pigs. We tested the effect of MH on circulatory failure during experimental endotoxemia.


Anesthetized pigs (65 ± 2 kg) were acutely instrumented (closed chest) with a series of catheters including 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). 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.


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 preserved systemic vascular resistance, 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 (bpm) increased in NT (128 ± 6* vs 97 ± 4) but fell in MH (79 ± 4*,† vs 98 ± 4). Spectral analysis of heart rate variability revealed no sympathetic activation during MH. In vitro, ventricular muscle strips from MH demonstrated an improved force response to isoproterenol compared to NT (all strips measured at 38 °C, 1 Hz).


The induction of MH during experimental endotoxemia attenuates sympathetic activation and improves myocardial beta-adrenergic responsiveness. These data imply that MH may serve to prevent sympathetic overstimulation and myocardial contractile failure during sepsis.

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