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SLEEP AND TEMPERATURE REGULATION
1Fractal Physiology, Max Planck Institute for Experimental Medicine, Göttingen, Germany; 2Center for Neurogenomics and Cognitive Research, Vrije Universiteit, Amsterdam, The Netherlands; 3Department of Zoology, University of Veterinary Medicine, Hannover, Germany
Submitted 10 July 2007 ; accepted in final form 14 November 2007
Djungarian or Siberian hamsters (Phodopus sungorus) acclimated to short photoperiod display episodes of spontaneous daily torpor with metabolic rate depressed by
70% and body temperature (Tb) reduced by
20°C. To study the cardiovascular adjustment to daily torpor in Phodopus, electrocardiogram (ECG) and Tb were continuously recorded by telemetry during entrance into torpor, in deep torpor, and during arousal from torpor. Minimum Tb during torpor bouts was
21°C, and heart rate,
349 beats/min at euthermy, displayed marked sinus bradyarrhythmia at
70 beats/min. Arousal was typically completed within
40 min, followed by a sustained posttorpor inactivity tachycardia (
540 beats/min). The absence of episodes of conduction block, tachyarrhythmia, or other forms of ectopy throughout the torpor cycle demonstrates a remarkable resistance to arrhythmogenesis. The ECG morphology lacks a distinct isoelectric interval following the QRS complex, and the ST segment resembles the ECG pattern in mice, with a prominent fast transient outward K+ current (Ito,f) determining the early phase of ventricular repolarization. During low-temperature torpor, the amplitudes of the QRS complex substantially increased, suggesting that in the euthermic state the terminal portion of ventricular depolarization is fused with the beginning of repolarization, low Tb acting to decorrelate the superposition between depolarization and repolarization by delaying the repolarization onset. Atrioventricular and ventricular conduction times were prolonged as function of Tb. In contrast, the QT vs. Tb relationship showed marked hysteresis indicating the operation of nonlinear control mechanisms whereby the rapid QT shortening during arousal results from additional mechanisms (probably sympathetic stimulation) other than temperature alone.
hibernation; electrophysiology; conduction; arrhythmia
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