Proceedings of The Physiological Society

University of Cambridge (2004) J Physiol 555P, C82

Communications

Does cardiovascular variability differ in normothermic and cold-acclimated anaesthetised rats during acute hypothermia?

R. Sabharwal, M. Shah, E. J. Johns* and S. Egginton

Departments of Physiology, University of Birmingham, UK and * University College Cork, Ireland


Heart rate variability (HRV) is described as the variation in R-R interval that occurs in consecutive waveforms of the electrocardiogram (ECG), which may act as a predictor of morbidity (Matthew et al. 2002). The power spectrum can be divided into low frequency (LF) and high frequency (HF) bands. In rats LF reflects sympathetic and parasympathetic control of blood pressure (BP), while HF is mostly due to parasympathetic stimulation and correlates with respiration frequency (Cerutti et al. 1991). The aim of the study was to compare HRV in rats without (normothermic, n = 10) and with prior exposure to lower ambient temperatures (cold-acclimated, n = 7) at normal core temperature (Tb) of 37°C, on cooling to Tb = 25°C (acute hypothermia) and on rewarming to Tb = 37°C.

Male Wistar rats, 295-310g, were anaesthetised with fluothane (2.5 % in O2) and α-chloralose/urethane (32/450 mg kg-1 I.V.). BP, ECG and ventilation were recorded and stored onto a computer for offline auto-spectral and cross-spectral analysis in the frequency domain. Deep oesophageal Tb was regulated by means of a thermostatted plate connected to a temperature control unit. Rats were killed humanely with an overdose of sodium pentobarbitone. Data (mean ± S.E.M.) were analysed using ANOVA and significance taken at P < 0.05.

At Tb = 25°C, in normothermic and cold-acclimated rats there was a similar prolongation of R-R interval by ~40 % (P < 0.001 vs. 37°C) and a shift of LF and HF range by 50 % and 35 % (P < 0.05 vs. 37°C). Hypothermia reduced total power by 26 % (P < 0.05) and 66 % (P < 0.01) reflecting central depression of neural outflow and decreased sympathetic control of peripheral blood flow suggested by reduced LF power by 21 % and 57 % (P < 0.05) in normothermic and cold-acclimated rats, respectively. In contrast, there was a moderate increase in HF power in normothermic rats (1.12 ± 0.33 ms2 vs. 1.07 ± 0.18 ms2) and a reduction in cold-acclimated rats (0.35 ± 0.09 ms2 vs. 0.82 ± 0.24 ms2) implying a higher vagal tone in former. In both groups, cross-spectral analysis between ECG, BP and ventilation revealed a high coherence between signals at HF at all Tb. Hypothermia increased the phase lag between ECG and BP signals by 60 % and 50 %, and between ECG and respiration by 35 % and 18 % (all P < 0.05) in normothermic and cold-acclimated rats, respectively. On rewarming all power spectra variables were completely restored to precooling levels.

These results suggest maintenance of cardio-respiratory coupling at lower Tb, and an intact autonomic system that rapidly restores physiological functions to steady-state levels on rewarming that was more efficient following cold-acclimation.

Where applicable, experiments conform with Society ethical requirements